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Expression of the T-Cell Surface Molecule CD2 and an Epitope-Loss CD2 Mutant to Define the Role of Lymphocyte Function-Associated Antigen 3 (LFA-3) in T-Cell Activation
Barbara E. Bierer, Andrew Peterson, James Barbosa, Brian Seed and Steven J. Burakoff
Proceedings of the National Academy of Sciences of the United States of America
Vol. 85, No. 4 (Feb. 15, 1988), pp. 1194-1198
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/30965
Page Count: 5
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To define the role of the CD2-lymphocyte function-associated antigen 3 (LFA-3) interaction in T-cell activation, we have expressed a cDNA encoding the human CD2 molecule in a murine antigen-specific T-cell hybridoma. Expression of the CD2 molecule greatly enhances T-cell responsiveness to antigen; this enhancement is inhibited by anti-CD2 and anti-LFA-3 monoclonal antibodies (mAbs). CD2+ hybridomas produce interleukin 2 in response to combinations of anti-CD2 mAbs 9.6 and 9-1 and, in the presence of mAb 9-1, to sheep erythrocytes or to the LFA-3 antigen. Furthermore, hybridomas expressing a mutant CD2 molecule that has lost mAb 9.6 binding do not exhibit the enhanced response to antigen or the ability to respond to LFA-3 plus mAb 9-1, but these hybridomas retain the ability to respond to combinations of anti-CD2 mAbs. The role of the CD2-LFA-3 interaction in T-cell activation and the potential for other physiologic ligands for CD2 are discussed.
Proceedings of the National Academy of Sciences of the United States of America © 1988 National Academy of Sciences