Autoimmune Diseases –
When the Immune System Turns Against Self
In
a healthy immune system, lymphocytes and antibodies respond to foreign
antigens while ignoring the body’s own molecules — a concept known as self–nonself
discrimination or immunological tolerance. This tolerance is
maintained by mechanisms such as central deletion of self‑reactive
lymphocytes in primary lymphoid organs and peripheral regulatory T‑cells
that suppress any autoreactive cells that escape deletion. When these tolerance
mechanisms fail — due to genetic predisposition, environmental triggers,
molecular mimicry, or immunoregulatory defects — the immune system begins
to attack self‑tissues, producing autoantibodies and/or autoreactive T‑cells
that damage organs. Such responses cause autoimmune diseases. (MSD
Manuals)
Autoimmune diseases can
be organ‑specific (targeting a single tissue) or systemic
(involving multiple organs) and may involve antibody‑mediated, immune‑complex,
or cell‑mediated mechanisms. (MSD
Manuals)
Mechanisms of
Autoimmunity
|
Mechanism |
Description |
|
Loss of Self‑Tolerance |
Defects in central and peripheral
tolerance allow autoreactive B and T cells to survive and attack self‑antigens.
(Wikipedia) |
|
Autoantibody Production |
B cells produce antibodies directed against self
antigens (autoantibodies) causing tissue damage via complement or receptor
interference. (NCBI) |
|
Cell‑Mediated Attack |
Autoreactive T cells destroy
cells directly (e.g., in Type 1 diabetes). (PSYCHOLOGICAL SCALES) |
|
Molecular Mimicry |
Pathogen antigens resemble self antigens, causing
cross‑reactivity. (PSYCHOLOGICAL SCALES) |
|
Inflammation and Cytokines |
Dysregulated cytokine responses
contribute to chronic inflammation. (SpringerLink) |
Examples of
Autoimmune Diseases
|
Disease |
Mechanism |
Key Features |
|
Paroxysmal Cold Hemoglobinuria (PCH) |
Autoantibody (biphasic IgG) binds
RBC antigen at cold, activates complement on warming. (Wikipedia) |
Intravascular hemolysis after
cold exposure |
|
Myasthenia Gravis |
Autoantibodies target acetylcholine receptors at
neuromuscular junction. (nsdl.niscpr.res.in) |
Muscle weakness, fatigue |
|
Systemic Lupus Erythematosus (SLE) |
Autoantibodies against DNA,
nuclear proteins → immune complexes, complement activation. (srrcvr.ac.in) |
Multi‑organ inflammation, rashes,
nephritis |
|
Type 1 Diabetes Mellitus |
T cell–mediated destruction of pancreatic β cells.
(Encyclopedia
Britannica) |
Hyperglycemia, insulin deficiency |
|
Hashimoto’s Thyroiditis |
Autoantibodies against thyroid
proteins cause tissue destruction. (MSD
Manuals) |
Hypothyroidism, goiter |
|
Rheumatoid Arthritis |
Autoimmune attack on joint synovium (immune
complexes, T cells). (MSD
Manuals) |
Chronic joint inflammation |
Immune Response
Patterns
Autoimmune
pathology can involve different hypersensitivity mechanisms:
- Type II:
Antibody‑mediated cell destruction (e.g., PCH, myasthenia gravis). (MSD
Manuals)
- Type III:
Immune complex deposition (e.g., SLE). (MSD
Manuals)
- Type IV:
T cell–mediated tissue destruction (e.g., Type 1 diabetes). (MSD
Manuals)
Summary
Autoimmune
diseases arise when self‑tolerance breaks down, allowing autoreactive
lymphocytes and autoantibodies to target host tissues. These disorders can
affect a single organ or be systemic, and their severity ranges from mild
chronic inflammation to severe multi‑organ damage. Genetics, environmental
triggers, and failures in immune regulation all contribute to disease
development. Early diagnosis and immunomodulatory therapies aim to restore
immune balance and reduce tissue injury. (MSD
Manuals)
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