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.org
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.