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  Indian J Med Microbiol
 

Figure 1 :The immunology of resolving infection and disease progression to Leishmania For both T helper 1 (TH1)- and TH2-cell differentiations, antigens are presented to naive CD4+ T cells by dendritic cells (DCs). The interaction of co-stimulatory molecules with their respective ligands, together with the local cytokine environment, promotes the differentiation of naive T cells into interferon- γ (IFN-γ)-secreting TH1 cells or interleukin-4 (IL-4)-secreting TH2 cells. In TH1-cell development, certain pathogens or pathogen-associated molecular patterns (PAMPs) trigger antigen-presenting cells, through toll-like receptors (TLRs), to secrete IL-12, which promotes the differentiation of naive T cells into IFN-γ-secreting TH1 cells. In TH2-cell development, the inability of antigen to activate DCs to produce IL-12 results in a default pathway of naive T-cell differentiation into IL-4-secreting TH2 cells

Figure 1 :The immunology of resolving infection and disease progression to Leishmania For both T helper 1 (TH1)- and TH2-cell differentiations, antigens are presented to naive CD4+ T cells by dendritic cells (DCs). The interaction of co-stimulatory molecules with their respective ligands, together with the local cytokine environment, promotes the differentiation of naive T cells into interferon- γ (IFN-γ)-secreting TH1 cells or interleukin-4 (IL-4)-secreting TH2 cells. In TH1-cell development, certain pathogens or pathogen-associated molecular patterns (PAMPs) trigger antigen-presenting cells, through toll-like receptors (TLRs), to secrete IL-12, which promotes the differentiation of naive T cells into IFN-γ-secreting TH1 cells. In TH2-cell development, the inability of antigen to activate DCs to produce IL-12 results in a default pathway of naive T-cell differentiation into IL-4-secreting TH2 cells