caa a22 4500 469073500 CHVBK 20180323132928.0 cr unu---uuuuu 170328e19920101xx s 000 0 eng 10.1007/BF01741054 doi (NATIONALLICENCE)springer-10.1007/BF01741054 The loss of class II MHC antigen expression by ras -transformed murine fibroblasts passaged as tumours correlates with increased tumorigenicity but is not mediated by T cells [Elektronische Daten] [Alan Morris, Richard Darley, Wendy Bateman] Summary: In several murine tumour systems, expression of class II major histocompatibility complex (MHC) antigens by tumour cells, either constitutive or inducible, correlates with reduced tumorigenicity as compared with equivalent class-II-negative cells, and CD4 phenotype T cells together with interferon γ (which induces the expression of class II) may be involved in the control of the proliferation of class-II-expressing tumours. This implies a potential T-cell-mediated selection pressure against class II expression. To test this possibility, we have repeatedly passaged as tumours in euthymic, syngeneic miceras-transformed murine fibroblast lines, which are class-II-inducible, to determine whether class-II-non-inducible variants are selected. We examined the expression of both class I and class II antigen in tumour cells re-established in vitro. It was found that the inducibility of class II, but not class I, expression rapidly diminished, correlating with augmented tumorigenicity. However, this loss of class II inducibility occurred in athymic as well as euthymic mice. Therefore, despite the fact that the tumorigenicity of these lines is augmented in euthymic mice depleted of CD4 T cells or interferon γ, we found no evidence of T-cell-mediated selection against class II expression. The loss of class II expression observed must be due to mechanisms other than immune selection. The possibility that this might result from other soluble factors modulating the response to interferon γ in vivo is discussed. Springer-Verlag, 1992 ras nationallicence MHC nationallicence interferon γ nationallicence Tumorigenicity nationallicence T cells nationallicence Morris Alan CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut Darley Richard CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut Bateman Wendy CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut Cancer Immunology, Immunotherapy Springer-Verlag 35/1(1992-01-01), 46-52 0340-7004 35:1<46 1992 35 262 https://doi.org/10.1007/BF01741054 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01741054 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Morris Alan CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut NATIONALLICENCE 700 1- Darley Richard CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut NATIONALLICENCE 700 1- Bateman Wendy CRC Research Group, Department of Biological Sciences, University of Warwick, CV4 7AL, Coventry, UK aut NATIONALLICENCE 773 0- Cancer Immunology, Immunotherapy Springer-Verlag 35/1(1992-01-01), 46-52 0340-7004 35:1<46 1992 35 262 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer