Ligation of the lymphocyte homing receptor CD44 triggers T-helper and cytolytic functions of human T cells.

Cytotechnology
R GalandriniA Velardi

Abstract

We show that antibodies to the CD44 molecule trigger proliferation of human CD3+/CD4+ T-cell clones. Such effect is IL2-dependent, as shown by IL2 production induced by anti-CD44 mAb and by inhibition of cell proliferation in the presence of anti-IL2 antibodies or cyclosporin A (CsA). Moreover, anti-CD44 mAb triggered human cytolytic CD4+ and CD8+ TCR α/β+ clones, and Vδ1 or Vδ2 TCR Y/δ+ clones to lyse Fc-gamma-R+ P815 cells and to release granule trypsin-like esterase enzymes. Anti-CD44 mAb-triggered proliferation and cytotoxicity were blocked by the PTK-inhibitor, genestein. In addition, ligation of the CD44 molecule induced tyrosine phosphorylation of proteins identical, by molecular weight, to those phosphorylated following anti-CD3 mAb-stimulation. Notably, anti-CD44 mAb does not induce tyrosine phosphorylation of a 21 kD protein (the phosphorylated zeta chain of the TcR molecular complex) typically observed upon anti-CD3 mAb stimulation.

References

Jun 1, 1991·Current Opinion in Immunology·G A van SeventerS Shaw

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Citations

Oct 17, 2002·Cellular Immunology·R GuyY Zilberman
Jan 1, 1996·Springer Seminars in Immunopathology·R L BolhuisJ W Gratama
Dec 28, 1999·Leukemia & Lymphoma·S IlangumaranD C Hoessli
Dec 6, 2002·The American Journal of Pathology·Qin WangClaire M Doerschuk

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