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Increased endogenous antigen presentation in the periphery enhances susceptibility to inflammation‐induced gastric autoimmunity in mice

How the immune system maintains peripheral tolerance under inflammatory conditions is poorly understood. Here we assessed the fate of gastritogenic T cells following inflammatory activation in vivo. Self‐reactive T cells (A23 T cells) specific for the gastric H+/K+ ATPase α subunit (HKα) were transferred into immunosufficient recipient mice and immunised at a site distant to the stomach with adjuvant containing the cognate HKα peptide antigen. Activation of A23 T cells by immunisation did not impact on either immune tolerance or protection from gastric autoimmunity in wild‐type BALB/c mice. However, increased presentation of endogenously derived HKα epitopes by dendritic cells (DCs) in the gastric lymph node of IE‐H+/K+β transgenic mice (IEβ) reduces A23 T‐cell tolerance to gastric antigens after inflammatory activation, with subsequent development of gastritis. While HKα‐specific A23 T cells from immunised wild‐type mice were poorly responsive to in vitro antigen specific activation, A23 T cells from immunised IEβ transgenic mice were readily re‐activated, indicating loss of T‐cell anergy. These findings show that DCs of gastric lymph nodes can maintain tolerance of pathogenic T cells following inflammatory stimulation and that the density of endogenous antigen presented to self‐reactive T cells is critical in the balance between tolerance and autoimmunity.