TABS, A T-CELL ACTIVATION ANTIGEN THAT INDUCES LFA-1-DEPENDENT AGGREGATION

We describe here a mAb, DATK44, which induces homotypic aggregation of TK1 cells (a CD8 lymphoma). The glycoprotein recognized by DATK44 is of approximate m.w. 50 kDa and is expressed by monocytes, neutrophils, and subsets of lymphocytes, as well as on the high endothelial venule in peripheral and mesenteric lymph nodes. We named this Ag TABS (T ce ll activation B cell subset Ag), as TABS appears on T lymphocyte activ ation and is expressed at low and high levels by B cells. TABS is diff erentially regulated during T lymphocyte development, CD4(+ve)CD8(+ve) thymocytes being TABS(high), while single positive CD4(+ve) and CD8(ve) thymocytes are TABS(dull) CD4(-ve)CD8(-ve) thymocytes are clearly split into dull and bright populations by the mAb. On exit from the th ymus, T lymphocytes cease to express TABS, but T lymphocyte activation results in re-expression of TABS. TABS also shows tight coregulation with heat stable Ag on resting lymphocytes, but coexpression of these two molecules is lost upon lymphocyte activation. DATK44-induced aggre gation of TK1 cells is temperature sensitive and blocked by pretreatme nt of the cells with metabolic inhibitors, genestein, dibutyl cAMP or cytochalasin B, while colchicine, staurosporin, sphingosine, okadaic a cid, and W7 are without effect. DATK44-induced TK1 cell aggregation ap pears to be mediated by the LFA-1 pathway, as aggregation is blocked b y anti-LFA-1 and anti-ICAM-1 mAbs but not by Abs capable of blocking C D44 and alpha(4) beta(7)-mediated adhesion. Thus, TABS appears to be a n adhesion inducer that selectively activates LFA-1-mediated lymphocyt e aggregation.