The article discusses how the evolution of somatic diversification of antigen receptor genes imposed changes in adaptive immune systems to mitigate the risk of autoimmunity. It suggests that early vertebrates had lower diversity in antigen receptors, allowing for the gradual development of tolerance mechanisms. The article highlights the significance of the thymic microenvironment, where medullary epithelial cells and peripheral mimetic cells help T cells become tolerant to self-antigens, affirming the critical role of these interactions in modern vertebrate immunity.
The emergence of somatic diversification of antigen receptor genes necessitated a reorganization of immune systems to prevent fatal autoimmunity linked to random receptor specificities.
Early vertebrates likely had lower initial diversity in antigen receptor repertoires, allowing time for the development of adequate tolerance mechanisms alongside increasing diversity.
Central tolerance in the thymus is facilitated by medullary epithelial cell expression of peripheral genes and peripheral mimetic cells, linking developing T cells to self-antigens.
Various peripheral cell types in the thymic microenvironment across vertebrates have demonstrated a tolerance-inducing role, confirming hypotheses about thymic mimetic cells established decades ago.
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