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Journal of Experimental Medicine, Vol 182, 1913-1919, Copyright © 1995 by Rockefeller University Press
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RR Brutkiewicz, JR Bennink, JW Yewdell and A Bendelac
Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892-0440, USA.
CD1 molecules consist of beta 2-microglobulin (beta 2m) noncovalently complexed to a non-major histocompatibility complex (MHC)-encoded monomorphic integral membrane protein homologous to MHC class I alpha chains. Little is known about the requirements for cell surface expression and T cell recognition of CD1. We inserted the mouse CD1.1 gene into vaccinia virus to create a recombinant virus expressing CD1.1 under the control of a viral promoter. Using this recombinant virus to infect normal or mutant cell lines, we found that the expression of molecules reactive with the CD1.1-specific monoclonal antibody 3C11 requires the expression of beta 2m but was not affected by the absence of the MHC-encoded peptide transporter (TAP). Consistent with these results, IL-2 production by the mCD1.1-specific T cell hybridoma DN32.D3 was induced by thymocytes from normal mice or mice with a homozygous deletion of the TAP1 gene, but not by thymocytes from mice with a homozygous deletion of the beta 2m gene. These results indicate that expression of functional mCD1.1 occurs in a beta 2m-dependent, TAP- independent manner.
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