T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues.
Two genes acting in concert control murine T cell I-Jk expression. We determined I-Jk expression with I-Jk--specific monoclonal antibodies WF8 .C12.8 and five others produced in our laboratory in a cytotoxicity assay. Previous experiments established that an H-2k gene and a chromosome 4 gene, Jt , regulate I-Jk expression. We show here that B10. HTT and B10.S( 9R ) do not differ at the H-2k locus required for I-Jk expression. Rather B10. HTT , like B10.A(3R), lacks some important non--H-2 gene (possibly Jt ). The intra--H-2k I-J--controlling locus maps to the right of the I-A subregion. The I-Jk determinant involves a carbohydrate structure associated with protein; inhibiting either protein synthesis or glycosylation prevents T cell I-Jk reexpression after proteolytic removal. Treatment with alpha-mannosidase destroys I-Jk determinants, implicating terminal alpha-D-mannosyl residues in the I-Jk epitope. Models for H-2 and Jt control of I-J expression are discussed.[1]References
- T cell surface I-J glycoprotein. Concerted action of chromosome-4 and -17 genes forms an epitope dependent on alpha-D-mannosyl residues. Klyczek, K.K., Cantor, H., Hayes, C.E. J. Exp. Med. (1984) [Pubmed]
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