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Figure 1: The current hypothesis by which T cells get activated and how the release of various mediators leads to the hyperproliferation of the keratinocyte. (ModiT ed from Mehlis and Gordon1, Krueger37) (A) T cell binds to an Antigen-Presenting Cell, (B) T cell receptor recognizes the antigen presented on MHC of the APC in an antigen speciT c interaction, (C) Non-antigen speciT c cell-interaction. The stimulation of both TCR and CD28 pathways lead to transcription of IL-2, TNF-, GM-CSF and IFN-, (D) T cell is rolling on the endothelium, (E) T cell surface proteins are activated, (F) T cell binds to the endothelium and diapedesis occurs, (G) Dermal Th1 cells release IFN- and other cytokines, which lead to increases expression of ins ammatory and adhesion proteins on keratinocytes, (H) Keratinocytes proliferate; synthesize angiogenic cytokines / chemokines that cause leukocyte trafT cking and increase leukocyte adhesion to the endothelial cells.

Figure 1: The current hypothesis by which T cells get activated and how the release of various mediators leads to the hyperproliferation of the keratinocyte. (ModiT ed from Mehlis and Gordon1, Krueger37) (A) T cell binds to an Antigen-Presenting Cell, (B) T cell receptor recognizes the antigen presented on MHC of the APC in an antigen speciT c interaction, (C) Non-antigen speciT c cell-interaction. The stimulation of both TCR and CD28 pathways lead to transcription of IL-2, TNF-, GM-CSF and IFN-, (D) T cell is rolling on the endothelium, (E) T cell surface proteins are activated, (F) T cell binds to the endothelium and diapedesis occurs, (G) Dermal Th1 cells release IFN- and other cytokines, which lead to increases expression of ins ammatory and adhesion proteins on keratinocytes, (H) Keratinocytes proliferate; synthesize angiogenic cytokines / chemokines that cause leukocyte trafT cking and increase leukocyte adhesion to the endothelial cells.