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题名:IFN2b stimulated release of IFN differentially regulates T cell and NK cell mediated tumor cell cytotoxicity ? ARTICLE
作者:Anamika Bose and Rathindranath Baral
来源:Immunology Letters[IF=2.301], Volume 108, Issue 1, 15 January 2007, Pages 68-77
URL :http://dx.doi.org/10.1016/j.imlet.2006.10.002
日期:070415
摘要: Anamika Bosea and Rathindranath Baral, a,

aDepartment of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S.P. Mookherjee Road, Kolkata 700026, India

Received 10 August 2006; revised 25 September 2006; accepted 10 October 2006. Available online 2 November 2006.

Summary

Interferon2b (IFN2b) augments the suppressed immune functions and peripheral blood mononuclear cell (PBMC) cytotoxicity of head and neck squamous cell carcinoma (HNSCC) patients by differential regulation of IFN, a pleotropic Th1 cytokine. In the present communication, we have examined the role of IFN in IFN2b initiated T and NK cell mediated cytotoxicity of tumor cells. IFN2b activates both T and NK cells to release IFN. IFN plays a crucial role in enhancing tumor cell cytotoxicity by T cells, but not by NK cells, as evidenced by killing of a oral (KB) and breast (MCF7) cancer cells, without affecting the killing of NK sensitive erythroleukemic K562 cells by IFN2b activated PBMC. IFN2b driven tumor cell cytotoxicity is related to the rectification of the downregulated expression of cytotoxic molecules, perforin, granzyme B and FasL in CD8+ T and CD56+ NK cells. Expression of IFN2b mediated perforin and granzyme B is dependent on IFN in T cells, but not in NK cells. However, expression of FasL in both T and NK cells is not dependent on IFN. In conclusion, IFN2b enhances suppressed T cell cytotoxicity of HNSCC patients by stimulating perforinCgranzyme B system, which is IFN dependent. IFN2b also induces the expression of perforinCgranzyme B system in NK cells, but this NK mediated cytotoxicity is IFN independent. 6.

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