In autoimmune diseases, the immune system detects the body's own molecules as foreign and triggers inflammation that damages specific tissues.
Mechanism
Synthesis from 3 studies
The immune system mistakenly identifies the body’s own molecules as foreign and sends cells to attack them. These cells release chemicals that cause swelling and damage in the affected tissue. Special cells try to stop the attack, but when they fail, the damage continues and becomes chronic.
Most probable mechanism
When the immune system encounters a molecule from the body’s own tissues, it mistakenly treats it as foreign. This causes specific immune cells to activate, multiply, and attack the tissue where that molecule is found. Other immune cells then suppress this attack, but when suppression fails, inflammation and damage occur in the affected organ.
Self-antigens are presented by antigen-presenting cells to naive T cells in lymphoid tissues, initiating activation of autoreactive CD4+ T cells.
Autoreactive CD4+ T cells differentiate into pro-inflammatory Th1 phenotypes, producing cytokines such as IFN-γ, TNF-α, and IL-12 that promote inflammation.
B cells recognize self-antigens via their B cell receptor, become activated, and differentiate into plasma cells that produce autoantibodies targeting the self-antigen.
Autoantibodies form immune complexes that deposit in tissues, activating complement and recruiting innate immune cells that cause local inflammation and structural damage.
Inflammatory cytokines and immune cell infiltration disrupt tissue barriers, such as the blood-brain barrier or joint synovium, enabling further immune cell entry and sustained damage.
Regulatory T cells are induced by inhibitory signals and immunosuppressive molecules such as IL-10 and rapamycin, which suppress autoreactive T and B cell responses and limit tissue destruction.
Failure of regulatory mechanisms allows persistent autoreactive cell activity, leading to chronic inflammation and irreversible tissue damage.
Evidence from Studies
Supporting (3)
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Suppression of Autoimmune Rheumatoid Arthritis with Hybrid Nanoparticles That Induce B and T Cell Tolerance to Self-Antigen.
Contradicting (0)
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