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Capsaicin induced regression of established tumors is in consequence of enhanced antigen presentation and alteration of stromal microenvironment
Author(s) -
Ghosh Amiya,
Basu Sreyashi
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1077.2
Subject(s) - tumor microenvironment , stromal cell , cancer research , cytotoxic t cell , immunotherapy , immune system , stroma , tumor progression , tumor antigen , antigen presentation , chemistry , cd8 , foxp3 , apoptosis , antigen , cytokine , immunology , t cell , medicine , cancer , in vitro , immunohistochemistry , biochemistry
Tumor microenvironment is crucial in preventing the immunological destruction of antigenic tumors. The phenomenon that intratumoral administration of Capsaicin (CP) into an established tumor results in retarded progression of the tumor led us to examine the potential function of CP in the tumor microenvironment. We have previously reported that CP causes apoptosis of tumor cells in vitro but a direct cytotoxic effect of CP responsible for tumor growth retardation seems unlikely as CP mediated immunotherapy is T cell mediated and tumor‐specific. In this report we confirm that CP injection specifically induces apoptosis in tumor cells in vivo. We show that CP induced apoptosis leads to increased sensitization of the surrounding stroma manifested by enhanced antigen presentation by stromal cells and thereby its destruction by tumor specific T‐cells. Most importantly we demonstrate that CP injection alters the tumor microenvironment with regards to tumor‐infiltrating T lymphocyte population as well as the cytokine milieu at the tumor site. CP treatment promotes antitumor immune response by blocking anti‐inflammatory cytokines and depletion of FoxP3+ suppressor T cells. Our study illustrates that CP mediated immunotherapy is attained by diverse immunological events initiated at the tumor environment.