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CD5 (OKT1) augments CD3-mediated intracellular signaling events in human T lymphocytes
Authors:Berney S M  Schaan T  Wolf R E  Kimpel D L  van der Heyde H  Atkinson T P
Affiliation:(1) Department of Medicine-Section of Rheumatology/Center of Excellence for Arthritis and Rheumatology, LSU School of Medicine at Shreveport, Shreveport, Louisiana, 71130-3932;(2) Department of Medicine-Section of Rheumatology/Center of Excellence for Arthritis and Rheumatology, LSU School of Medicine at Shreveport, Shreveport, Louisiana, 71130-3932;(3) Department of Microbiology, LSU School of Medicine at Shreveport, Shreveport, Louisiana, 71130;(4) Department of Pediatrics-Division of Clinical and Developmental Immunology, University of Alabama at Birmingham, Birmingham, Alabama, 35294
Abstract:CD5 is expressed on thymocytes, all mature T cells, and a subset of mature B cells, and probably contributes to T-cell–B-cell adhesion. We assessed whether CD5-crosslinking by mAb augments T-cell stimulation. Plate-bound anti-CD5 or anti-CD3 mAb alone had no effect on any of the assessed activation parameters of resting T cells. However, concomitant signaling through both CD5 and CD3 by plate-bound antibodies resulted in marked increases in T-cell surface CD69 expression and T-cell metabolism, as assessed by the T cell's ability to reduce 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxylmethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) to formazen. In addition, simultaneous cross-linking of CD5 and CD3 caused a significant (p < 0.001) increase in phosphatidylinositol hydrolysis in resting T cells compared to stimulation with anti-CD3 mAb alone or anti-CD3 mAb plus anti-CD5 isotype control antibody. These results indicate that CD5 augments signaling through CD3 and consequently functions as a costimulatory molecule for resting T cells.
Keywords:CD5  T cell  cellular activation  signal transduction  adhesion molecule
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