What is the role of peripheral tolerance in autoimmune disease prevention?
Peripheral tolerance helps prevent autoimmune diseases by regulating immune cells outside the thymus and bone marrow, ensuring that they do not attack body's own tissues. It maintains immune homeostasis by inactivating or eliminating self-reactive T and B cells that have escaped central tolerance.
How does peripheral tolerance differ from central tolerance?
Peripheral tolerance occurs outside primary lymphoid organs, ensuring mature self-reactive immune cells do not cause autoimmune responses, while central tolerance happens in the thymus and bone marrow, eliminating self-reactive immature lymphocytes during their development to prevent autoimmunity.
How is peripheral tolerance maintained in the immune system?
Peripheral tolerance is maintained through mechanisms such as anergy, regulatory T cells (Tregs), and deletion. Anergy involves rendering self-reactive T and B cells inactive, Tregs suppress immune responses against self-antigens, and deletion refers to the removal of these cells. These processes prevent autoimmune responses and maintain immune homeostasis.
Can peripheral tolerance be disrupted, and what are the consequences?
Yes, peripheral tolerance can be disrupted, leading to the activation of self-reactive lymphocytes. This disruption can result in autoimmune diseases, where the immune system mistakenly attacks the body's own tissues, potentially causing chronic inflammation and tissue damage.
What are the key mechanisms involved in peripheral tolerance?
Key mechanisms of peripheral tolerance include the induction of regulatory T cells (Tregs), anergy (functional inactivation) of self-reactive T or B cells, deletion of autoreactive lymphocytes by apoptosis, and immune suppression via cytokines like IL-10 and TGF-beta from Tregs.