Understanding Autoimmune Disease: NIAID
Article title: Understanding Autoimmune Disease: NIAID
Conditions: Autoimmune Diseases, B-cell, autoantibody, antibody, antigen, lymphocyte, macrophage, neutrophil, T-cell, Rheumatoid arthritis, Multiple sclerosis, Type 1 diabetes mellitus, Inflammatory Bowel Disease, Crohn's disease, Lupus, Psoriasis, Scleroderma, Thyroid diseases, Autoimmune Thyroid diseases
Source: NIAID
Contents
Preface
What
Are Autoimmune Diseases? Who Is
Affected by Autoimmune Diseases? What
Are the Causes of Autoimmune Diseases? Are
they contagious? Are
they inherited? What
other factors may influence the development of autoimmune diseases?
How
Does the Immune System Work? T and
B Cells Macrophages
and Neutrophils MHC and
Co-Stimulatory Molecules Cytokines
and Chemokines Antibodies
Autoantibodies
Immune
Complexes and the Complement System Genetic
Factors How
Are Autoimmune Diseases Diagnosed? How
Are Autoimmune Diseases Treated? What
Are Some Examples of Autoimmune Diseases? Rheumatoid
Arthritis Multiple
Sclerosis Immune-Mediated
or Type 1 Diabetes Mellitus Inflammatory
Bowel Diseases Systemic
Lupus Erythematosus Psoriasis
Scleroderma
Autoimmune
Thyroid Diseases What
Research Is Under Way on Autoimmune Diseases? Resources
Glossary
Understanding Autoimmune Diseases
Preface
This booklet contains information about
autoimmune diseases.
You will not find everything there is to know about autoimmune diseases here,
however. In fact, the information presented here may prompt you to think of more
questions about autoimmune diseases because autoimmune diseases are complex.
We have tried to anticipate which terms will need further definition and
clarification. Those terms, when they first appear in the text, are in italics.
Italicized words and phrases are defined in the
Glossary
at the end of the booklet.
You will find more in-depth and detailed
resources at your local library or through your health care provider. The
Internet is a valuable source of information as well. Start by doing a search on
the National Institutes of Health (NIH) Web site at
http://www.nih.gov/ for information on the broad
range of research conducted by NIH, including autoimmune diseases.
What Are Autoimmune Diseases?
The word "auto" is the Greek word for self. The immune system is a
complicated network of cells and cell components (called
molecules)
that normally work to defend the body and eliminate infections caused by
bacteria, viruses, and other invading microbes. If a person has an autoimmune
disease, the immune system mistakenly attacks self, targeting the cells,
tissues, and organs of a person's own body. A collection of immune system cells
and molecules at a target site is broadly referred to as inflammation.
There are many different autoimmune diseases, and they can each affect
the body in different ways. For example, the autoimmune reaction is directed
against the brain in multiple sclerosis and the gut in Crohn's disease. In other
autoimmune diseases such as systemic lupus erythematosus (lupus), affected
tissues and organs may vary among individuals with the same disease. One person
with lupus may have affected skin and joints whereas another may have affected
skin, kidney, and lungs. Ultimately, damage to certain tissues by the immune
system may be permanent, as with destruction of insulin-producing cells of the
pancreas in Type 1 diabetes mellitus.
Who Is Affected by Autoimmune Diseases?
Many of the autoimmune diseases are rare. As a group, however,
autoimmune diseases afflict millions of Americans. Most autoimmune diseases
strike women more often than men; in particular, they affect women of working
age and during their childbearing years.
Some autoimmune diseases occur
more frequently in certain minority populations. For example, lupus is more
common in African-American and Hispanic women than in Caucasian women of
European ancestry. Rheumatoid arthritis and scleroderma affect a higher
percentage of residents in some Native American communities than in the general
U.S. population. Thus, the social, economic, and health impact from autoimmune
diseases is far-reaching and extends not only to family but also to employers,
co-workers, and friends.
What Are
the Causes of Autoimmune Diseases? Are they contagious? No autoimmune disease has ever
been shown to be contagious or "catching." Autoimmune diseases do not spread to
other people like infections. They are not related to AIDS, nor are they a type
of cancer.
Are they inherited?
The genes people inherit contribute to their susceptibility for developing an
autoimmune disease. Certain diseases such as psoriasis can occur among several
members of the same family. This suggests that a specific gene or set of genes
predisposes a family member to psoriasis. In addition, individual family members
with autoimmune diseases may inherit and share a set of abnormal
Examples of Autoimmune
Diseases:
(listed by the Main Target Organs)
Nervous Systems:
Gastrointestinal System:
Multiple sclerosis
Crohn's Disease
Myasthenia gravis
Ulcerative colitis
Autoimmune neuropathies
Primary biliary cirrhosis
such as Guillain-Barré
Autoimmune hepatitis
Autoimmune ureitis
Endocrine Glands:
Blood:
Type 1 or immune mediated
Autoimmune hemolytic anemia
diabetes mellitus
Pernicious anemia
Grave's Disease
Autoimmune thrombocytopenia
Hashimoto's thyroiditis
Autoimmune oophoritis and
Blood Vessels:
orchitis
Temporal artertis
Autoimmune disease of the
Anti-phospholipid syndrome
adrenal gland
Vasculitides such as
Wegener's granulomatosis
Multiple Organs Including the
Behcet's disease
Musculoskeletal Systems:*
Rheumatoid arthritis
Skin:
Systemic lupus erythematosus
Psoriasis
Scleroderma
Dermatitis herpetiformis
Polymyositis, dermatomyositis
Pemphigus vulgaris
Spondyloarthropathies such as
Vitiligo
ankylosing spondylitis
Sjogren's syndrome
*These diseases are also called connective
tissue (muscle, skeleton, tendons, fascia, etc.)
diseases.genes, although they may
develop different autoimmune diseases. For example, one first cousin may have
lupus, another may have dermatomyositis, and one of their mothers may have
rheumatoid arthritis.
The development of an autoimmune disease may be
influenced by the genes a person inherits together with the way the person's
immune system responds to certain triggers or environmental influences.
What other factors may influence the
development of autoimmune diseases? Some autoimmune diseases are
known to begin or worsen with certain triggers such as viral infections.
Sunlight not only acts as a trigger for lupus but can worsen the course of the
disease. It is important to be aware of the factors that can be avoided to help
prevent or minimize the amount of damage from the autoimmune disease. Other less
understood influences affecting the immune system and the course of autoimmune
diseases include aging, chronic stress, hormones, and pregnancy.
How Does the Immune System
Work? The immune system defends the body from attack
by invaders recognized as foreign. It is an extraordinarily complex system that
relies on an elaborate and dynamic communications network that exists among the
many different kinds of immune system cells that patrol the body. At the heart
of the system is the ability to recognize and respond to substances called
antigens whether they are infectious agents or part of the body (self
antigens).
T and B Cells Most
immune system cells are white blood cells, of which there are many types.
Lymphocytes are one type of white blood cell, and two major classes of
lymphocytes are
T cells and
B cells. T cells are critical
immune system cells that help to destroy infected cells and coordinate the
overall immune response. The T cell has a molecule on its surface called the
T-cell receptor. This receptor interacts with molecules called
MHC
(major histocompatibility complex). MHC molecules are on the surfaces of
most other cells of the body and help T cells recognize antigen fragments. B
cells are best known for making antibodies. An antibody binds to an antigen and
marks the antigen for destruction by other immune system cells. Other types of
white blood cells include
macrophages and
neutrophils.
Macrophages and Neutrophils
Macrophages and neutrophils circulate in the blood and survey the body
for foreign substances. When they find foreign antigens, such as bacteria, they
engulf and destroy them. Macrophages and neutrophils destroy foreign antigens by
making toxic molecules such as
reactive oxygen intermediate molecules.
If production of these toxic molecules continues unchecked, not only are the
foreign antigens destroyed, but tissues surrounding the macrophages and
neutrophils are also destroyed. For example, in individuals with the autoimmune
disease called Wegener's granulomatosis, overactive macrophages and neutrophils
that invade blood vessels produce many toxic molecules and contribute to damage
of the blood vessels. In rheumatoid arthritis, reactive oxygen intermediate
molecules and other toxic molecules are made by overproductive macrophages and
neutrophils invading the joints. The toxic molecules contribute to inflammation,
which is observed as warmth and swelling, and participate in damage to the
joint.
MHC and Co-Stimulatory Molecules
MHC molecules are found on all cell surfaces and are an active part of
the body's defense team. For example, when a virus infects a cell, a MHC
molecule binds to a piece of a virus (antigen) and displays the antigen on the
cell's surface. Cells that have the capability of displaying antigen with MHC
are called antigen-presenting cells. Each MHC molecule that displays an antigen
is recognized by a matching or compatible T-cell receptor. Thus, an
antigen-presenting cell is able to communicate with a T cell about what
may be occurring inside the cell. However, for the T cell to respond to a
foreign antigen on the MHC, another molecule on the antigen-presenting cell must
send a second signal to the T cell. A corresponding molecule on the surface of
the T cells recognizes the second signal. These two secondary molecules of the
antigen-presenting cell and the T cell are called co-stimulatory molecules.
There are several different sets of co-stimulatory molecules that can
participate in the interaction of antigen-presenting cell with a T cell.
Once the MHC and the T-cell receptor interact, and the co-stimulatory
molecules interact, there are several possible paths that the T cell may take.
These include T cell activation, tolerance, or T cell death. The subsequent
steps depend in part on which co-stimulatory molecules interact and how well
they interact. Because these interactions are so critical to the response of the
immune system, researchers are intensively studying them to find new therapies
that could control or stop the immune system attack on self tissues and organs.
Cytokines and Chemokines
One way T cells can respond after the interaction of the MHC and the
T-cell receptor, and the interaction of the co-stimulatory molecules, is to
secrete cytokines and chemokines. Cytokines are proteins that may cause
surrounding immune system cells to become activated, grow, or die. They also may
influence non-immune system tissues. For example, some cytokines may contribute
to the thickening of the skin that occurs in people with scleroderma.
Chemokines are small cytokine molecules that attract cells of the immune
system. Overproduction of chemokines contributes to the invasion and
inflammation of the target organ, which occurs in autoimmune diseases. For
example, overproduction of chemokines in the joints of people with rheumatoid
arthritis may result in invasion of the joint space by destructive immune system
cells such as macrophages, neutrophils, and T cells.
Antibodies B cells are another critical
type of immune system cell. They participate in the removal of foreign antigens
from the body by using a surface molecule to bind the antigen or by making
specific antibodies that can search out and destroy specific foreign antigens.
However, the B cell can only make antibodies when it receives the appropriate
command signal from a T cell. Once the T cell signals the B cell with a type of
cytokine that acts as a messenger molecule, the B cell is able to produce a
unique antibody that targets a particular antigen.
Autoantibodies In some autoimmune
diseases, B cells mistakenly make antibodies against tissues of the body (self
antigens) instead of foreign antigens. Occasionally, these autoantibodies either
interfere with the normal function of the tissues or initiate destruction of the
tissues. People with myasthenia gravis experience muscle weakness because
autoantibodies attack a part of the nerve that stimulates muscle movement. In
the skin disease pemphigus vulgaris, autoantibodies are misdirected against
cells in the skin. The accumulation of antibodies in the skin activates other
molecules and cells to break down, resulting in skin blisters.
Immune Complexes and the Complement
System When many antibodies are bound to antigens in the
bloodstream, they form a large lattice network called an
immune
complex. Immune complexes are harmful when they accumulate and initiate
inflammation within small blood vessels that nourish tissues. Immune complexes,
immune cells, and inflammatory molecules can block blood flow and ultimately
destroy organs such as the kidney. This can occur in people with systemic lupus
erythematosus.
A group of specialized molecules that form the
complement system helps to remove immune complexes. The different types
of molecules of the complement system, which are found in the bloodstream and on
the surfaces of cells, make immune complexes more soluble. Complement molecules
prevent formation and reduce the size of immune complexes so they do not
accumulate in the wrong places (organs and tissues of the body). Rarely, some
people inherit defective genes for a complement molecule from their parents.
Because these individuals cannot make a normal amount or type of complement
molecule, their immune systems are unable to prevent immune complexes from being
deposited in different tissues and organs. These people develop a disease that
is not autoimmune but resembles lupus erythematosus.
Genetic Factors Genetic factors can affect an
individual's immune system and its responses to foreign antigens in several
ways. Genes determine the variety of MHC molecules that individuals carry on
their cells. Genes also influence the potential array of T-cell receptors
present on T cells. In fact, some MHC genes are associated with autoimmune
diseases. However, genes are not the only factors involved in determining a
person's susceptibility to an autoimmune disease. For example, some individuals
who carry disease-associated MHC molecules on their cells will not develop an
autoimmune disease.
How Are
Autoimmune Diseases Diagnosed? The diagnosis of an
autoimmune disease is based on an individual's symptoms, findings from a
physical examination, and results from laboratory tests. Autoimmune diseases can
be difficult to diagnose, particularly early in the course of the disease.
Symptoms of many autoimmune diseases—such as fatigue—are nonspecific. Laboratory
test results may help but are often inadequate to confirm a diagnosis.
If an individual has skeletal symptoms such as joint pain and a positive
but nonspecific lab test, she or he may be diagnosed with the confusing name of
early or "undifferentiated" connective tissue disease. In this case, a physician
may want the patient to return frequently for follow up. The early phase of
disease may be a very frustrating time for both the patient and physician. On
the other hand, symptoms may be short-lived, and inconclusive laboratory tests
may amount to nothing of a serious nature.
In some cases, a specific
diagnosis can be made. A diagnosis shortly after onset of a patient's symptoms
will allow for early aggressive medical therapy; and for some diseases, patients
will respond completely to treatments if the reason for their symptoms is
discovered early in the course of their disease.
Although autoimmune
diseases are chronic, the course they take is unpredictable. A doctor cannot
foresee what will happen to the patient based on how the disease starts.
Patients should be monitored closely by their doctors so environmental factors
or triggers that may worsen the disease can be discussed and avoided and new
medical therapy can be started as soon as possible. Frequent visits to a doctor
are important in order for the physician to manage complex treatment regimens
and watch for medication side effects.
How Are Autoimmune Diseases Treated?
Autoimmune diseases are often chronic, requiring lifelong care and
monitoring, even when the person may look or feel well. Currently, few
autoimmune diseases can be cured or made to "disappear" with treatment. However,
many people with these diseases can live normal lives when they receive
appropriate medical care.
Physicians most often help patients manage the
consequences of inflammation caused by the autoimmune disease. For example, in
people with Type 1 diabetes, physicians prescribe insulin to control blood sugar
levels so that elevated blood sugar will not damage the kidneys, eyes, blood
vessels, and nerves. However, the goal of scientific research is to prevent
inflammation from causing destruction of the insulin-producing cells of the
pancreas, which are necessary to control blood sugars.
On the other
hand, in some diseases such as lupus or rheumatoid arthritis, medication can
occasionally slow or stop the immune system's destruction of the kidneys or
joints. Medications or therapies that slow or suppress the immune system
response in an attempt to stop the inflammation involved in the autoimmune
attack are called immunosuppressive medications. These drugs include
corticosteroids (prednisone), methotrexate, cyclophosphamide, azathioprine, and
cyclosporin. Unfortunately, these medications also suppress the ability of the
immune system to fight infection and have other potentially serious side
effects.
In some people, a limited number of immuno-suppressive
medications may result in disease remission. Remission is the medical term used
for "disappearance" of a disease for a significant amount of time. Even if their
disease goes into remission, patients are rarely able to discontinue
medications. The possibility that the disease may restart when medication is
discontinued must be balanced with the long-term side effects from the
immunosuppressive medication.
A current goal in caring for patients with
autoimmune diseases is to find treatments that produce remissions with fewer
side effects. Much research is focused on developing therapies that target
various steps in the immune response. New approaches such as therapeutic
antibodies against specific T cell molecules may produce fewer long-term side
effects than the chemotherapies that now are routinely used.
Ultimately,
medical science is striving to design therapies that prevent autoimmune
diseases. To this end, a significant amount of time and resources are spent
studying the immune system and pathways of inflammation.
What Are Some Examples of Autoimmune
Diseases? Rheumatoid
Arthritis In people with rheumatoid arthritis, the immune
system predominantly targets the lining (synovium) that covers various joints.
Inflammation of the synovium is usually symmetrical (occurring equally on both
sides of the body) and causes pain, swelling, and stiffness of the joints. These
features distinguish rheumatoid arthritis from osteoarthritis, which is a more
common and degenerative "wear-and-tear" arthritis.
Currently available
therapy focuses on reducing inflammation of the joints with anti-inflammatory or
immunosuppresssive medications. Sometimes, the immune system may also target the
lung, blood vessels, or eye; occasionally patients may also develop symptoms of
other autoimmune diseases such as Sjogren's the inflammation, itching, and
scaling. For more severe cases, oral medications are used. Psoriasis is common
and may affect more than 2 out of 100 Americans. Psoriasis often runs in
families.
Multiple Sclerosis
Multiple sclerosis is a disease in which the immune system targets nerve
tissues of the central nervous system. Most commonly, damage to the central
nervous system occurs intermittently, allowing a person to lead a fairly normal
life. At the other extreme, the symptoms may become constant, resulting in a
progressive disease with possible blindness, paralysis, and premature death.
Some medications such as beta interferon are helpful to people with the
intermittent form of multiple sclerosis.
In young adults, multiple
sclerosis is the most common disabling disease of the nervous system. Multiple
sclerosis afflicts 1 in 700 people in this country. Researchers continue to
search for triggers of the disease.
Immune-Mediated or Type 1 Diabetes Mellitus
Type 1 diabetes mellitus results from autoimmune destruction of the
insulin-producing cells of the pancreas. Insulin is required by the body to keep
the blood sugar (glucose) level under control. High levels of glucose are
responsible for the symptoms and the complications of the disease. However, most
of the insulin-producing cells are destroyed before the patient develops
symptoms of diabetes. Symptoms include fatigue, frequent urination, increased
thirst, and possible sudden confusion.
Type 1 diabetes mellitus is
usually diagnosed before the age of 30 and may be diagnosed as early as the
first month of life. Together with Type 2 diabetes (not considered an autoimmune
disease), diabetes mellitus is the leading cause of kidney damage, loss of
eyesight, and leg amputation. Close control of sugar levels decreases the rate
at which these events occur. There is a genetic predisposition to Type 1
diabetes, which occurs in 1 out of 800 people in the United States. Among
individuals who have a close relative with Type 1 diabetes, those at high risk
for developing disease can be identified. Efforts are now under way to evaluate
prevention strategies for these family members at risk.
Inflammatory Bowel Diseases This medical term is
used for both Crohn's disease and ulcerative colitis, two diseases in which the
immune system attacks the gut (intestine). Patients may have diarrhea, nausea,
vomiting, abdominal cramps, and pain that can be difficult to control. Illness
in afflicted individuals can result from intestinal inflammation and from side
effects of the drugs used for the disease. For example, daily use of high-dose
corticosteroid (prednisone) therapy, which is needed to control severe symptoms
of Crohn's disease, can predispose patients to infections, bone thinning
(osteoporosis), and fractures. For patients with ulcerative colitis, surgical
removal of the lower intestine (colon) will eliminate the disease and their
increased risk for colon cancer. More than 1 in 500 Americans has some type of
inflammatory bowel disease.
Systemic Lupus
Erythematosus Patients with systemic lupus erythematosus
most commonly experience profound fatigue, rashes, and joint pains. In severe
cases, the immune system may attack and damage several organs such as the
kidney, brain, or lung. For many individuals, symptoms and damage from the
disease can be controlled with available anti-inflammatory medications. However,
if a patient is not closely monitored, the side effects from the medications can
be quite serious. Lupus occurs in 1 out of 2,000 Americans and in as many as 1
in 250 young, African-American women.
Psoriasis Psoriasis is an immune system
disorder that affects the skin, and occasionally the eyes, nails, and joints.
Psoriasis may affect very small areas of skin or cover the entire body with a
buildup of red scales called plaques. The plaques are of different sizes,
shapes, and severity and may be painful as well as unattractive. Bacterial
infections and pressure or trauma to the skin can aggravate psoriasis. Most
treatments focus on topical skin care to relieve the inflammation, itching, and
scaling. For more severe cases, oral medications are used. Psoriasis is common
and may affect more than 2 out of 100 Americans. Psoriasis often runs in
families.
Scleroderma
This autoimmune disease results in thickening of the skin and blood
vessels. Almost every patient with scleroderma has Raynaud's, which is a spasm
of the blood vessels of the fingers and toes. Symptoms of Raynaud's include
increased sensitivity of the fingers and toes to the cold, changes in skin
color, pain, and occasionally ulcers of the fingertips or toes. In people with
scleroderma, thickening of skin and blood vessels can result in loss of movement
and shortness of breath or, more rarely, in kidney, heart, or lung failure. The
estimated number of people with any type of scleroderma varies from study to
study but may range from 1 to 4 affected individuals for every 10,000 Americans
(or as many as 1 out of 2500 individuals).
Autoimmune Thyroid Diseases Hashimoto's
thyroiditis and Grave's disease result from immune system destruction or
stimulation of thyroid tissue. Symptoms of low (hypo-) or overactive (hyper-)
thyroid function are nonspecific and can develop slowly or suddenly; these
include fatigue, nervousness, cold or heat intolerance, weakness, changes in
hair texture or amount, and weight gain or loss. The diagnosis of thyroid
disease is readily made with appropriate laboratory tests. The symptoms of
hypothyroidism are controlled with replacement thyroid hormone pills; however,
complications from over- or under-replacement of the hormone can occur.
Treatment of hyperthyroidism requires long-term anti-thyroid drug therapy or
destruction of the thyroid gland with radioactive iodine or surgery. Both of
these treatment approaches carry certain risks and long-term side effects.
Autoimmune thyroid diseases afflict as many as 4 out of 100 women and are
frequently found in families where there are other autoimmune diseases.
What Research Is Under Way on
Autoimmune Diseases? The National Institute of
Allergy and Infectious Diseases (NIAID) supports research studies on the
function of the immune system in various diseases. A basic understanding of the
human immune system is central to the understanding of the development of an
autoimmune disease (disease pathogenesis). Scientists searching for ways to
prevent and treat autoimmune disease are studying disease pathogenesis and
investigating new ways to modify the immune system.
Specifically,
investigators supported by NIAID are focusing on: 1) studies of the immune
system during the progression of an autoimmune disease; 2) analysis of the
influence of genetics on autoimmune disease expression and progression; 3) the
role of infectious agents in autoimmune diseases; 4) studies of animal models of
autoimmune diseases; and 5) the effects of therapeutic intervention on the
immune system in an autoimmune disease.
In addition, studies of a
specific autoimmune disease such as multiple sclerosis can provide new and
additional insights into the pathogenesis of autoimmune diseases affecting other
organ systems. Therefore, NIAID also supports studies on specific autoimmune
diseases in cooperation with other Institutes of the National Institutes of
Health that focus on organ-specific autoimmune diseases.
Resources
National Institutes of Health (NIH) Resources
The following NIH components support medical research and/or provide
information on varying aspects of autoimmune diseases.
National
Institute of Allergy and Infectious Diseases Office of Communications
Bldg. 31/Rm. 7A50
31 Center Drive, MSC 2520
Bethesda, MD 20892-2520
(301) 496-5717
http://www.niaid.nih.gov/publications/
and
http://www.niaid.nih.gov/clintrials/default.htm
(for
clinical trials information)
National Institute of
Arthritis and Musculoskeletal and Skin Diseases Information
Clearinghouse/NIH
1 AMS Circle
Bethesda, MD 20892-3675
Fast Facts:
(301) 881-2731 (to receive information by fax)
Clearinghouse: (301) 495-4484
http://www.nih.gov/niams/healthinfo/
National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) Information Clearinghouse
1 Information Way
Bethesda, MD
20892-3560
Diabetes, Digestive, and Kidney Diseases Information:
(301)
654-3810
NIDDK Information Office (Thyroid Diseases) Bldg.
31/Rm. 9A04
31 Center Drive
Bethesda, MD 20892-3560
(301) 496-3583
http://www.niddk.nih.gov/
National Institute of Neurological Disorders and Stroke
Office of Scientific and Health Reports
P.O. Box 5801
Bethesda, MD
20824
(301) 496-5751
http://www.ninds.nih.gov/ NIH
Clinical Center Patient Recruitment and Referral Center—for specific NIH
clinical trials information
4 West Drive, MSC 2655
Quarters 15 D-2
Bethesda, MD 20892-2655
(301) 411-1222
http://clinicalstudies.info.nih.gov/referring_patient.html
Office of Rare Diseases, NIH Bldg. 31/Rm. 1B03
31 Center
Drive
Bethesda, MD 20892
(301) 402-4336
http://rarediseases.info.nih.gov/ord/
Other Resources Sponsored by the Department of Health and Human
Services National Health Information Center (800)
336-4797 or (301) 565-4167
Health Finder:
http://www.healthfinder.gov/
Combined Health Information Database http://chid.nih.gov/ Private
Sector Organizations The following list is astarting point for
additional information on autoimmune diseases. Many of the organizations have
extensive educational resources, local chapters, and support groups. The
Internet Web site of many organizations can refer you to other disease-oriented
groups (for example, the Arthritis Foundation has alink to the Lupus
Foundation).
American Autoimmune Related Diseases Association
15475 Gratiot Avenue
Detroit, MI 48205
(800) 598-4668 or (313)
371-8600
http://www.aarda.org/
American Diabetes Association 1660 Duke Street
Alexandria, VA 22314
(800) 232-3472 or (703) 549-1500
http://www.diabetes.org/ American
Liver Foundation 1425 Pompton Avenue
Cedar Grove, NJ 07009
(800)
233-0179 and (973) 256-2550
American Thyroid Association Montefiore
Medical Center 111 East 210th Street
Bronx, NY 10467
Fax: (718)
882-6085
http://www.thyroid.org/
Arthritis Foundation 1650 Bluegrass Lakes Pkwy.
Alpharetta, GA 30009
(800) 283-7800 or (800) 207-8633
http://www.arthritis.org/
Crohn's and Colitis Foundation of America National
Headquarters
386 Park Avenue South, 17th Floor
New York, NY 10016-8804
(800) 932-2423
(800) 343-3637 (Warehouse)
http://www.ccfa.org/ Juvenile
Diabetes Foundation International 120 Wall Street
New York, NY
10005-4001
(800) JDF-CURE or (800) 533-2873
http://www.jdf.org/ Lupus Foundation
of America 1300 Piccard Drive, Suite 200
Rockville, MD 20850-4303
(800) 558-0121 and (301) 670-9292
http://www.lupus.org/ Myasthenia
Gravis Foundation of America 222 S. Riverside Plaza, Suite 1540
Chicago, IL 60606
(800) 541-5454 or (312) 258-0522
http://www.myasthenia.org/
Myositis Association of America 755 Cantrell Avenue
Suite
C
Harrisonburg, VA 22801
(540) 433-7686
http://www.myositis.org/ National
Alopecia Areata Foundation 710 CStreet, Suite 11
San Rafael, CA
94901-3853
or
P.O. Box 150760
San Rafael, CA 94915-0760
(415)
456-4644
Fax: (415) 456-4274
http://www.alopeciaareata.com/
National Multiple Sclerosis Society 733 Third Avenue, 6th
Floor
New York, NY 10017-3288
(800) 344-4867 or (212) 986-3240
Fax:
(212) 986-7981
http://www.nmss.org/
e-mail: ire@nmss.org
National Organization for Rare Disorders
P.O. Box 8923
New Fairfield, CT 06812-1783
(800) 999-6673
http://www.rarediseases.org/
National Psoriasis Foundation 6600 SW 92nd Avenue, Suite 300
Portland, OR 97223
(800) 723-9166 or (503) 244-7404
http://www.psoriasis.org/
National Sjogren's Syndrome Association 5815 N. Black Canyon
Highway, Suite 103
Phoenix, AZ 85015-2200
(602) 433-9844
http://www.sjogrens.com/ National
Vitiligo Foundation P.O. Box 6337
Tyler, TX 75703
(903) 531-0074
Fax: (903) 531-9767
http://www.nvfi.org/ Sjogren's
Syndrome Foundation 333 N. Broadway
Jericho, NY 11753
1-800-4-SJOGRENS or (516) 933-6365
http://www.sjogrens.com/
Spondylitis Association of America P.O. Box 5872
Sherman
Oaks, CA 91413
(800) 777-8189 or (888) 777-1594
http://www.spondylitis.org/
The S.L.E. Foundation 149 Madison Avenue, Suite 205
New
York, NY 10016
(800) 745-8787
http://www.lupus.org/ United
Scleroderma Foundation 89 Newbury Street, Suite 201
Danvers, MA
01923
800) 722-HOPE
Fax: (978) 750-9902
http://www.scleroderma.org/
Wegener's Foundation 3705 South George Mason Drive, Suite
1813
Falls Church, VA 22041
(703) 931-5852
Wegener's
Granulomatosis Support Group P.O. Box 28660
Kansas City, MO
64188-8668
(800) 277-9474
Fax: (816) 436-8211
http://www.wgsg.org/ Glossary
antibody: a molecule (also called an immunoglobulin) produced
by a B cell in response to an antigen. The binding of antibody to antigen leads
to the antigen's destruction.
antigen: a substance or molecule
that is recognized by the immune system. The molecule can be from a foreign
material such as a bacterium or virus, or the molecule can be from the same
organism (one's own body) and called a self antigen.
antigen-presenting cell: a cell that displays an antigen with
an MHC molecule on the cell surface.
autoantibody: antibodies
that are made against the body's own organs and tissues rather than foreignparts
of bacteria or viruses.
autoimmune disease: condition in which
the immune system mistakenly attacks the body's own organs and tissues.
B cell: a type of lymphocyte, which is an immune system cell.
Among its many roles, the B cell produces antibodies that bind antigens.
cells: the building blocks that make up tissues, organs, and
bloodstream of the body. Immune system cells normally move throughout the
bloodstream and reside temporarily in the lymph nodes, spleen, and thymus.
chemokine: a substance manufactured by cells and tissues, that
stimulates movement and activation of immune system cells to the area where the
chemokine is produced.
clinical trial: a prospective,
scientific evaluation in human volunteers of a treatment regimen, device, or
procedure used for the prevention, diagnosis, or treatment of a disease.
complement system: this series of molecules works together to
perform many immune system functions. For example, the complement system helps
to dissolve and remove immune complexes and to kill foreign cells.
co-stimulatory molecules: pairs of molecules on the surfaces of
two cells that work together with the MHC and T-cell receptors of those cells.
The co-stimulatory molecules help to stimulate or decrease the immune response
produced by the two cells.
cytokines: chemical substances that
have varied effects on many cells of the body. For example, some cytokines can
cause growth and activation of immune system cells.
gene: a
unit of genetic material that is inherited from a parent. A gene carries the
directions that a cell uses to perform a specific function.
immune
complex: a cluster of interlocking antigens and antibodies forming a large
network of molecules.
inflammation: a collection of immune
system cells and molecules that invade tissues and organs as part of an immune
system response.
lymphocyte: a type of white blood cell of the
immune system. T cells and B cells are lymphocytes that look similar under the
microscope but have different functions.
macrophage: a type of
white blood cell that functions as a patrol cell and engulfs and kills foreign
infectious invaders.
MHC (major histocompatibility complex)
molecules: molecules that are found on cell surfaces and display antigen;
the antigen-MHC molecules may then interact with a T-cell receptor.
molecule: a small physical unit made up of chemical substances
such as proteins, sugars or fats. Molecules are the building blocks of a cell.
neutrophil: a type of immune system cell that combats
infectious agents, in particular bacteria. Neutrophils contain granules filled
with potent chemicals that can destroy bacteria or other nearby cells when the
chemicals are released.
reactive oxygen intermediate molecules:
toxic molecules that are released by immune cells and help to destroy invading
microbes. These molecules can sometimes destroy healthy body tissues nearby.
T-cell: a type of lymphocyte. T cells have T-cell receptors
and, sometimes, co-stimulatory molecules on their cell surfaces. The T cell
helps to orchestrate the immune system and can issue "orders" for other cells to
make cytokines and chemokines.
T-cell receptor: a molecule
found on the surface of T cells. The T-cell receptor can recognize and interact
with a corresponding MHC molecule that is displaying an antigen.
tolerance: a state in which the T cell can no longer respond to
antigen.
