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  Indian J Med Microbiol
 

Figure 1: Immune checkpoints are upregulated during Leishmania donovani infection. For keeping self-tolerance, controlling the immune response, and reducing tissue damage, binding of Leishmania antigen-MHC II complex which is located on antigen presenting cell (APC) to T cell receptor (TCR) that is present on T cells promotes expression of the immune check points; PD-1 and CTLA-4 on the surface of T cells. PD-1 binds to PDL-1 and PDL-2, while CTLA-4 binds to B7-1 and B7-2, with greater affinity than the co-stimulatory molecule CD28. The net result is reduction of T cell proliferation and decreased pro-inflammatory cytokines production.

Figure 1: Immune checkpoints are upregulated during <i>Leishmania donovani</i> infection. For keeping self-tolerance, controlling the immune response, and reducing tissue damage, binding of <i>Leishmania</i> antigen-MHC II complex which is located on antigen presenting cell (APC) to T cell receptor (TCR) that is present on T cells promotes expression of the immune check points; PD-1 and CTLA-4 on the surface of T cells. PD-1 binds to PDL-1 and PDL-2, while CTLA-4 binds to B7-1 and B7-2, with greater affinity than the co-stimulatory molecule CD28. The net result is reduction of T cell proliferation and decreased pro-inflammatory cytokines production.