Polarized immune responses differentially regulate cancer development.
Tumor-associated immune responses assert varied responses toward developing neoplasms that can either act to eradicate malignant cells via engagement of potent cytotoxic programs or alternatively enhance tumor growth through release of multifunctional pro-tumor mediators. Seemingly paradoxical, these disparate activities reflect a continuum of polarization (or activation) states possible for distinct leukocyte subsets that demonstrate tissue, organ, and tumor selectivity. Herein, we review clinical and experimental studies investigating cellular and molecular mechanisms utilized by neoplastic tissues to alternatively polarize immune responses that favor either pro- or anti-tumor immunity.
Johansson
Magnus
M
Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Denardo
David G
DG
Coussens
Lisa M
LM
D000818:Animals; D019070:Cell Lineage / Q000276:immunology; D002471:Cell Transformation, Neoplastic / Q000276:immunology*; D006801:Humans; D007111:Immunity, Cellular; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology; D051379:Mice; D009369:Neoplasms / Q000098:blood supply / Q000276:immunology* / Q000473:pathology / Q000628:therapy; D009389:Neovascularization, Pathologic; D051381:Rats; D011961:Receptors, Fc / Q000276:immunology; D013491:Suppressor Factors, Immunologic / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology
D011961:Receptors, Fc; D013491:Suppressor Factors, Immunologic; D051193:Toll-Like Receptors