Omar D Perez1, 2, Dennis Mitchell1, Gina C Jager1, Sharon South1, Chris Murriel3, Jacqueline McBride4, Lee A Herzenberg5, Shigemi Kinoshita6
& Garry P Nolan1, 21
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA.
2
The Baxter Laboratory of Genetic Pharmacology, Stanford University School of Medicine, Stanford, California 94305, USA.
3
Department of Molecular Pharmacology, Stanford University School of Medicine, Stanford, California 94305, USA.
4
Department of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305, USA.
5
Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA.
6
Department of Dermatology, Center for Immunology, The University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9069, USA.
Correspondence should be addressed to Garry P Nolan gnolan@stanford.edu
2 integrin chain and release of Jun-activating binding protein 1 (JAB-1), and mediated signaling of kinase Erk1/2 through cytohesin-1. Dominant negatives of both JAB-1 and cytohesin-1 inhibited interleukin 2 production and impaired T helper type 1 differentiation. LFA-1 stimulation lowered the threshold of T cell activation. Thus, LFA-1 signaling contributes to T cell activation and effects T cell differentiation.
-2 integrin-mediated adhesion through both ARF-GEF function and interaction with LFA-1
