W. Kasinrerk et al., CD99 monoclonal antibody induce homotypic adhesion of Jurkat cells throughprotein tyrosine kinase and protein kinase C-dependent pathway, IMMUNOL LET, 71(1), 2000, pp. 33-41
CD99 is a 32 kDa cell surface glycoprotein which is involved in cell adhesi
on. Engagement of the CD99 molecule by CD99 monoclonal antibodies has been
shown to induce homotypic aggregation of various cell types. By using a new
ly established CD99 monoclonal antibody, MT99/3, we show here that LFA-1/CA
M-1 independent cell adhesion pathways are activated via CD99. Engagement o
f the CD99 molecule by MT99/3 induced homotypic cell aggregation of Jurkat
T-cells within 30 min reaching its maximal level within 4 h. The Jurkat cel
l aggregation was not blocked by addition of CD11a (LFA-1) and CD54 (ICAM-1
) mAbs. Furthermore, MT99/3 treatment did not alter the expression of LFA-1
and ICAM-1 molecules. Induction of Jurkat homotypic aggregation by MT99/3
was, however blocked by the protein kinase C inhibitor, sphingosine. the pr
otein tyrosine kinase inhibitor, genistein, and by actin filament polymeriz
ation blocking agent, cytochalasin B. Thus, these observations suggest that
CD99 can mediate beta 2-integrin independent cell adhesion that depends on
activation of protein kineses and reorganization of the cytoskeleton. (C)
2000 Elsevier Science B.V. All rights reserved.