The mechanisms involved in the inhibition of growth of a human B lymphoma cell line, B104, by anti‐MHC class II antibodies (Ab) were compared with those in anti‐IgM Ab‐induced B104 growth inhibition. Two anti‐MHC class II Ab, L227 and 2.06, inhibited the growth of B104 cells, although 2.06, but not L227, needed to be further cross‐linked with a goat anti‐mouse IgG Ab (GAM) to show the effect. L227 induced an increase in intracellular free Ca2+ concentration ([Ca2+]i) from the intracellular pool and little or no protein tyrosine phosphorylation. phosphatidyl inositol turnover, or expression of Egr‐1 mRNA, whereas 2.06 plus GAM induced an increase in [Ca2+]i from both the intracellular and, in particular, the extracellular pools. The inhibition of B104 cell growth induced by anti‐MHC class II Ab was Ca2+ ‐independent and not inhibited by actinomycin D or cyclosporin A, and cell cycle arrest at the G2/M interphase was not observed. These features are very different from those observed in B104 cell death induced by anti‐IgM Ab. Neither DNA fragmentation nor the morphology of apoptosis was observed. These findings demonstrate that cross‐linking of MHC class II molecules transduced the negative signals through intracellular mechanisms different from those present in the cross‐linking of surface IgM.
|ジャーナル||Immunology and Cell Biology|
|出版ステータス||Published - 1994 6|
ASJC Scopus subject areas
- Immunology and Allergy
- Cell Biology