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Differential Expression of Major Histocompatibility Complex Class II Variants in Cells Infiltrating the Meth A Sarcoma
Author(s) -
Lill-Tove Busund,
Mette Kjær Killie,
Francisco León,
J. Fandrem,
Kristian Bartnes
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00530.x
Subject(s) - meth , major histocompatibility complex , biology , sarcoma , differential (mechanical device) , histocompatibility , immunology , expression (computer science) , cancer research , medicine , human leukocyte antigen , pathology , antigen , computer science , chemistry , monomer , organic chemistry , acrylate , engineering , programming language , aerospace engineering , polymer
CD4 + T cells are involved in immune responses against the Meth A sarcoma and infiltrate tumours arising from Meth A cells inoculated intradermally in (BALB/c × C57BL/6)F 1 (H‐2 d/b ) mice. In order to investigate whether the prerequisites for tumour antigen presentation to CD4 + T cells are fulfilled within the malignant lesion, expression of class II major histocompatibility complex (MHC) molecules and the costimulatory ligand B7 were examined. The I‐A b and I‐E d allomorphs were abundantly expressed by virtually all B cells and 50% of macrophages infiltrating the tumours. In striking contrast, the I‐A d variant was hardly detectable. This pattern of class II expression appeared to be unique for the tumour microenvironment. Thus the proportion of I‐A d+ spleen B cells and peritoneal macrophages did not significantly differ from the proportion expressing I‐A b and I‐E d , and these extratumoral I‐A d+ cells stained as brightly as did cells from healthy mice. Expression of B7 was weak by tumour‐infiltrating cells. The profound capacity of the Meth A sarcoma to confer low local I‐A d and B7 expression might preclude T‐cell‐dependent anti‐tumour immune responses and thus promote survival of malignant cells. Whereas MHC class II genes are generally found to be co‐ordinately transcribed, this study demonstrates that the expression of MHC class II allelic variants can be differentially regulated in vivo .