HSPs and γδ T Cell

It has been shown that HSPs are released after cell death or necrosis of tumors and can activate a plethora of non-APC such as al3 T cells, γδ T cells, NK cells NK-T cells, mast cells, and platelets. The γδ T-cells recognize HSPs expressed on the cell surface of tumor cells and become activated. The activated γδ T cells lyse the tumor cells with specificity, which further stimulate adaptive immunity against cancer due to the release of intracellular materials containing HSPs complexed with tumor antigens. In this way, γδ T-cells, such as intraepithelial T-lymphocytes in the epithelium keep vigil for any transformation in neighboring cells or nascent transformed tumor cells, and efficiently eradicate them, completing the elimination phase of the immunosurveillance mechanism.

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Several bacterial or parasitic infections activate specific γδ T cell subsets that are capable of responding to Hsp60 and Hsp70. These γδ T cell subpopulations have been shown to have an essential role in the protection of the host against infections, for example in experimental Listeria monocytogenes, Mycobacteria tuberculosis, or Plasmodium malaria infections. Thus, when the immune surveillance system detects Hsp molecules on the surface of host cells, it recognizes these cells as pathogen-afflicted and induces a cytotoxic immune response that results in the elimination of the affected host cells.