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- W4313385621 abstract "Abstract Type 1 diabetes (T1D) is a largely T cell mediated autoimmune disease that destroys the beta cells of the pancreatic islets. Initiation of T1D requires T cell activation in the pancreatic lymph node, and then activated T cells must enter the islets to destroy beta cells. The requirements for lymphocyte entry into islets are not fully understood. We show that lymphocyte entry into previously infiltrated islets is dependent on CD11c+ cells in the islets. T cells and B cells transferred prior to CD11c+ cell depletion were able to enter the islets; whereas, short-term CD11c+ cell depletion rapidly prevented further entry. CD11c+ cells are highly efficient antigen presenters; however, entry into the islets was not reliant on antigen for either activated or naïve T cells. An alternative role for CD11c+ cells in lymphocyte entry into the islets is the production of chemokines and cytokines, which can have direct chemotactic effects on lymphocytes or can activate vascular endothelium. CD11c+ cells in the islets express high levels of CXCL9, a chemoattractant for T and B lymphocytes. CXCR3, the receptor for CXCL9, is present on both T and B lymphocytes in the islets. We hypothesize that CD11c+ cells facilitate lymphocyte recruitment to the islets through a combination of chemokine production and activation of the islet vascular endothelium. Chemokine and cytokine production by CD11c+ cells may be targeted therapeutically for the treatment of T1D to prevent T cell entry into remaining or transplanted islets." @default.
- W4313385621 created "2023-01-06" @default.
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- W4313385621 date "2016-05-01" @default.
- W4313385621 modified "2023-09-27" @default.
- W4313385621 title "CD11c+ cells are required for lymphocyte trafficking into previously infiltrated pancreatic islets during type 1 diabetes." @default.
- W4313385621 doi "https://doi.org/10.4049/jimmunol.196.supp.119.19" @default.
- W4313385621 hasPublicationYear "2016" @default.
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