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Nonorgan-specific Disorders
1.Genetic factors
2.Age
3.Exogenous Factors
Features of Non-organ specific AID
Serological and clinical overlap may occur within families.
The damage is related to immune complex deposition in
the tissues.
Well-established tolerance in health to the antigens
concerned makes it difficult to reproduce the disease
experimentally.
Natural animal models such as NZB ,ice and SLE dogs are
the only way of studying the disease experimentally.
Treatment has to be immunosupressive therapy and
anitinflammmatory drugs and plasmapheresis.
Rheumatoid arthritis (RA)
The majority of adult RA patients have IgM
rheumatoid factor (RF) in their serum detectable
by routine laboratory tests with sensitized sheep
cells aor latex agglutination. A portion of juvenile
patients, however, have only IgG-RF, which is not
detectable by these routine tests. They have
milder disease, without rheumatoid nodules and
vasculitis that complicate severe seropositive RA.
Either type of RF, however, can induce
immunecomplex-mediated arthritis.
Signs and Symptoms
RA is a chronic, usually progressive
inflammatory disorder of the joints. It is
however, a highly variable disease that
ranges from a mild illness of brief duration to
a progressive, destructive polyarthritis
associated with systemic vasculitis.
Three Distinct Stages:
1.Initiation os synovitis by the primary etiologic
facter.
2.Subsequent immunologic events that
perpetuate the initial inflammatory reaction
3.Transition of an Inflammatory reactuion in the
synovium to a proliferative destructive
process of tissue.
SystemiC lupus erythematosus (SLE)
This multisystemic disease is caused by over-
reactivity of the T helper and B cell systems due
to suboptimal function of the T suppressor cell
circuit. A wide range of antibodies against
somatic epitopes therefore develop, for instance
against nucleoproteins, lymphocytes, RBC,
platelets, clotting factors, immunoglobulins and
neurones.
The tissue damage in SLE is either
caused by the immune complex
mechanism, as in skin, kidney, and
joints, or by direct cytotoxic damage,
as in the case of the blood elements
and neurones, resulting in
lymphopenia, hemolytic anemia,
thrombocytopenia, bleeding tendency
and neurological symptoms
respectively. In some cases of SLE anti-
lymphocyte antibodies appear to cross-
react with CNS antigens, causing
neurological symptoms and with
trophoblastic tissues, causing repeated
Immunologic Manifestations
Diagnostic evaluation
The manifestations of SLE expressed in
laboratory findings are numerous.
Histologic,
hematologic
serologic abnormalities
The tissue damage in SLE is either
caused by the immune complex
mechanism, as in skin, kidney, and
joints, or by direct cytotoxic damage,
as in the case of the blood elements
and neurones, resulting in
lymphopenia, hemolytic anemia,
thrombocytopenia, bleeding tendency
and neurological symptoms
respectively. In some cases of SLE anti-
lymphocyte antibodies appear to cross-
react with CNS antigens, causing
neurological symptoms and with
trophoblastic tissues, causing repeated
References
Immunology Simplified, 2nd Edition by
Bowry
Immunology and Serology in Laboratory
Medicine, 2nd Edition by Mary Louise
Turgeon
Basic and Clinical Immunology by D.P
Stites et. al.