Cutting edge: tumor secreted heat shock-fusion protein elicits CD8 cells for rejection.
نویسندگان
چکیده
The endoplasmic reticulum resident heat shock protein gp96 chaperons peptides, including those derived from tumor Ags, on their way to presentation by MHC class I. Replacement of the endoplasmic reticulum retention signal of gp96 with the Fc portion of murine IgG1 generated a secretory form of gp96, gp96-Ig. Tumor cells secreting gp96-Ig exhibited decreased tumorigenicity and increased immunogenicity in vivo and were rejected after initial growth. Rejection required CD8 T cells during the priming and effector phase. CD4 T cells were not required for rejection in either phase. Carrageenan, a compound known to inactivate macrophages in vivo, did not diminish CD8-mediated tumor rejection. Therefore, immunization with tumors secreting gp96-Ig generates efficient tumor-rejecting CD8 CTL without requirement for CD4 or macrophage help. In contrast, immunization with purified, tumor-derived gp96 or with irradiated tumor cells requires both.
منابع مشابه
Perforin Is Required for Innate and Adaptive Immunity Induced by Heat Shock Protein Gp96 of CD8 CTL in response to heat shock protein gp96- peptide comlexes, indicating an essential function for perforin-mediated lysis in the nascent NK and CD8 CTL
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عنوان ژورنال:
- Journal of immunology
دوره 163 10 شماره
صفحات -
تاریخ انتشار 1999