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Autoimmune Diseases

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  What Are Autoimmune Diseases?
  Who Is Affected by Autoimmune Diseases?
  What Are the Causes of Autoimmune
  Are they contagious?
  Are they inherited?
  What other factors may influence the
development of autoimmune diseases?
Graphic: Cells How Does the Immune System Work?
T and B Cells
Macrophages and Neutrophils
MHC and Co-Stimulatory Molecules
Cytokines and Chemokines
Immune Complexes and the Complement System
Genetic Factors
  How Are Autoimmune Diseases
  How Are Autoimmune Diseases Treated?
Graphic: woman standing in the sun, holding flowers What Are Some Examples of Autoimmune
Rheumatoid Arthritis
Multiple Sclerosis
Immune-Mediated or Type 1 Diabetes Mellitus
Inflammatory Bowel Diseases
Systemic Lupus Erythematosus
Autoimmune Thyroid Diseases
  What Research Is Under Way on
Autoimmune Diseases?
  May 1998 NIH Publication No.
  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
for information on the broad range of research conducted by NIH,
including autoimmune diseases.
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
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.
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 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
Examples of
Autoimmune Diseases:

(Listed by the Main Target Organ)

  Multiple sclerosis   Crohn’s Disease
  Myasthenia gravis   Ulcerative colitis
  Autoimmune neuropathies   Primary biliary cirrhosis
     such as Guillain-Barré   Autoimmune hepatitis
  Autoimmune uveitis    
      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 arteritis   Autoimmune disease of the
  Anti-phospholipid syndrome      adrenal gland
  Vasculitides such as    
     Wegener’s granulomatosis   Multiple Organs Including the
  Behcet’s disease   Musculoskeletal System:*
      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.
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.
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
Cells and molecules of the
immune system protect the nose from attack by a virus.
Graphic: Immune System showing Antibody, B Cell, T Cell, Cytokine, Complement, Macrophage, and Virus
Graphic: T Cell (lymphocyte) with a T-cell receptor on its surface

T cell (lymphocyte) with a T-cell receptor on its surface
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
A macrophage engulfing a
bacterium and releasing packets of toxic molecules (reactive
oxygen intermediates) that break down and destroy the bacterium.
Graphic: Macrophage Engulfing Bacteria showing Macrophage, Antibody, Bacterium, and Packet of toxic molecules
  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.
Upper left: a virus attacking a
nerve cell. Lower right: a T cell with a T-cell receptor
recognizing a piece of a virus (antigen) on the MHC of the
infected nerve cell.
Graphic: Virus Attacking Nerve Cell showing Virus, MHC, Virus Reproducing, and Viral Antigen
  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.
An antigen-presenting cell (for
example, a macrophage) with a foreign antigen on its MHC is
recognized by a T-cell receptor. In addition, co-stimulatory
molecules on the antigen-presenting cell and the T cell interact.
Graphic: Antigen-Presenting Cell showing Foreign antigen on MHC, T-cell receptor, and co-stimulatory molecules
  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.
After the antigen-presenting
cell and T cell interact through the MHC, T-cell receptor and co-stimumlatory
and molecules, the T cell becomes activated, sending cytokine
signals to other cells.
Graphic: Activated T Cell and other T Cells showing Cytokine signals.
  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.

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.
A T cell sends messenger
molecules, e.g. cytokines, to the B cell, which allows the B cell
to start making antibodies.
T Cell Sending Messenger molecules to B Cell which  produces antibodies

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

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
A large immune complex. A large immune complex showing antigen and antibody
  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.
If immune complexes accumulate
in the kidney, they may promote movement of other inflammatory
cells and molecules into the kidney.
Kidney Filter Unit showing  Immune Complex
  A group of specialized molecules that form the complement
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.
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
Doctor & Patient 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.
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.
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.
An inflamed joint—the
synovium—is attacked by cells and molecules of the immune
Graphic: Inflamed Joint showing Bone, Normal synovium, normal cartilage, eroding cartliage, joing capsule, inflammatory immune cells, and proliferating and disentigrating synovium
  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.
Pancreas and islet cell Immune-Mediated or Type 1 Diabetes

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.
Sunlight is one of the triggers
of lupus and can worsen the progression of the disease.
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
Graphic: woman standing in sun holding flowers 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 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

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
The thyroid gland affect many
parts of the body.
Diagram of human body showing theThyroid Gland and the areas it affects: eyes, muscle, bone, brain, hair, and heart
  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.
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.
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

autoimmune disease: condition in which the immune system
mistakenly attacks the body’s own organs and tissues.
B Cell 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

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 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 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

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.

Last Updated June 30, 2003 (ere)