Figure 1
Figure 1. Pathophysiology of GVHD: the donor T cell is encountering a host antigen-presenting cell (APC: monocyte/dendritic cell). The APC is activated by the conditioning treatment with radiation and chemotherapy; kit may also be activated by infections: viral via Toll-like receptor-9 (TLR9), bacterial infection via lipopolysaccharide (LPS), CD14, and TLR4. The interaction is regulated by recognition of mHA in the context with CD4 and HLA class II. The reaction is stimulated by costimulatory molecules CD40-CD40 ligand, B7.1-CD28, and adhesion molecules ICAM and LFA3. Cytokine secretion includes tumor necrosis factor-α and IL-6 by the APC and IFN-γ and GM-CSF by the T cell.

Pathophysiology of GVHD: the donor T cell is encountering a host antigen-presenting cell (APC: monocyte/dendritic cell). The APC is activated by the conditioning treatment with radiation and chemotherapy; kit may also be activated by infections: viral via Toll-like receptor-9 (TLR9), bacterial infection via lipopolysaccharide (LPS), CD14, and TLR4. The interaction is regulated by recognition of mHA in the context with CD4 and HLA class II. The reaction is stimulated by costimulatory molecules CD40-CD40 ligand, B7.1-CD28, and adhesion molecules ICAM and LFA3. Cytokine secretion includes tumor necrosis factor-α and IL-6 by the APC and IFN-γ and GM-CSF by the T cell.

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