Immunology

T.L. Walunas, D.J. Lenschow, C.Y. Bakker, P.S. Linsley, G.J Freeman, J.M. Green, C.B. Thompson, J.A. Bluestone, "CTLA-4 can function as a negative regulator of T-cell activation," Immunity, 1:405-13, 1994. (Cited in more than 40 publications as of February 1996) Comments by Jeffrey A. Bluestone, University of Chicago, and Craig B. Thompson, Howard Hughes Medical Institute, University of Chicago TURN-OFF:Jeffrey Bluestone hopes to understand how the immune system shuts itself down. In this

Written byJeffrey Bluestone
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T.L. Walunas, D.J. Lenschow, C.Y. Bakker, P.S. Linsley, G.J Freeman, J.M. Green, C.B. Thompson, J.A. Bluestone, "CTLA-4 can function as a negative regulator of T-cell activation," Immunity, 1:405-13, 1994. (Cited in more than 40 publications as of February 1996)

Comments by Jeffrey A. Bluestone, University of Chicago, and Craig B. Thompson, Howard Hughes Medical Institute, University of Chicago


TURN-OFF:Jeffrey Bluestone hopes to understand how the immune system shuts itself down.
In this paper, Jeffrey Bluestone and his collaborators at the University of Chicago, along with colleagues at New York-based Bristol-Myers Squibb Co. and Harvard University, examined the role of CTLA-4, an immune system protein.

"CTLA-4 was of interest because it was a homolog-a gene with the same structure, chromosomal location, ligands-of a molecule called CD28," explains Craig B. Thompson, a professor of medicine and a Howard Hughes Medical Institute investigator at the University of Chicago.

CD28 has intrigued immunologists because ...

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