AUTO-IMMUNITY
*EXPLAINED*
The Normal Immune System Response.
The inflammatory process is a byproduct of the body's
immune system, which fights infection and heals wounds
and injuries:
When an injury or an infection occurs, white blood cells
are mobilized to rid the body of any foreign proteins,
such as a virus.
In the process the surrounding area becomes inflamed and
some healthy tissue is injured.
Under normal conditions, the immune system has other
factors that control and limit this inflammatory process.
The Infection Fighters.
The primary infection-fighting units are two types of
white blood cells: lymphocytes and leukocytes.
T-cells, however, are further categorized as killer
T-cells or helper T-cells (TH cells).
Killer T-cells directly attack antigens, such as viruses,
that occur in any cells that contains a nucleus.
Helper T-Cells.
For some unknown reason, the T-cells become overactive
and mistake the body's own cells as an antigen and
trigger a series of immune responses to destroy the false
enemy.
The Helper T-cells normally stimulate B-cells to produce
antibodies.
In this case, however they appear to direct the B-cells
to produce autoantibodies, which are directed against the
body's own cells.
Antibodies come in five types: IgM, IgG, IgA,
IgD, or IgE. The autoantibody (anti
nuclear antibody aka ANA) in
SLE appears to be derived from IgG.
Autoantibodies.
In the majority of patients with SLE, antinuclear
antibodies (ANA) are the specific autoantibodies that
attack the nucleus and DNA of the patient's healthy
cells.
Experts have identified two subtypes of ANA that are
specific only to SLE patients:anti-double strand and
anti-single strand DNA.
Anti-DNA.
An autoantibody called anti-double stranded DNA (anti-ds
DNA) may play a critical role in the process.
Studies suggest that these antibodies specifically attack
a protein in the kidney, which researchers suspect may
also occur in other tissues that are affected by SLE,
such as in the skin, joints, and brain.
Other autoantibodies may also be
involved,
(eg - Anti-Ro (SSA) and Anti-Sm antibodies).
These autoantibodies may be involved in the photosensitivity issues
experienced by some SLE patients.
Antiphospholipid
Antibodies
About 50% of SLE patients also have these APS antibodies.
They attack phospholipids, fatty compounds found in cell
membranes throughout the body.
Antiphospholipid antibodies increase the risks for blood
clots and may be responsible for narrowing of and
irregularities in blood vessels and low blood cell
counts.
Antiphospholipid antibodies are linked with miscarriage,
kidney, heart, cerebral, and eye problems in SLE
patients.
Cytokines.
TH-cells also secrete or stimulate the production of
powerful immune factors called cytokines.
In small amounts, cytokines are indispensable for
healing.
If overproduced, they can cause inflammation that occurs
in parts of the body beyond the joints, which can produce
fever, shock, and even organ damage, such as the liver.
Researchers are currently interested in interferon alpha;
some scientists believe high levels of this cytokine may
underlie the autoimmune response in SLE.
Complement.
Another immune factor of high interest in SLE is
complement.
This is comprised of more than 30 proteins and is
important for defending and regulating the immune
response against foreign cells.
Inherited deficiencies in certain complement components
(C1q, C1r, C1s, C4, and C2) have long been associated
with SLE. Deficiencies may contribute to SLE autoimmune
disorder and inflammatory responses.
Immune complex is the end product of the
intense immune activity.
It consists of autoantibodies and antigens, leftover
debris when the battle is over.
This debris accumulates and is deposited in the kidneys,
blood vessels, joints, and other sites where it further
incites the immune system to produce inflammation and
tissue damage.
Blood also can be affected by autoimmune
disorder. In autoimmune hemolytic anemia,
red blood cells are prematurely destroyed by antibodies.
Other autoimmune diseases of the blood include:
autoimmune thrombocytopenic purpura and
autoimmune neutropenia.
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