title: Mechanisms involved in the inhibition of growth of a human B lymphoma cell line, B104, by anti-MHC class II antibodies.
abstract: 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 Ca(2+)-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.
authors.affiliation: Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Higaki
authors.forename: D
authors.initials: D
authors.lastname: Hata
authors.forename: S
authors.initials: S
authors.lastname: Kanazashi
authors.forename: Y
authors.initials: Y
authors.lastname: Horiguchi
authors.forename: K
authors.initials: K
authors.lastname: Yamaoka
authors.forename: Y
authors.initials: Y
authors.lastname: Ohshima
authors.forename: K M
authors.initials: KM
authors.lastname: Kim
authors.forename: T
authors.initials: T
authors.lastname: Heike
authors.forename: M
authors.initials: M
authors.lastname: Mayumi
mesh_terms: D000911:Antibodies, Monoclonal; D001402:B-Lymphocytes / Q000166:cytology*; D002118:Calcium / Q000502:physiology; D002453:Cell Cycle / Q000276:immunology; D002455:Cell Division / Q000276:immunology*; D004268:DNA-Binding Proteins / Q000235:genetics; D051766:Early Growth Response Protein 1; D006681:HLA-D Antigens / Q000276:immunology*; D006801:Humans; D017874:Immediate-Early Proteins; D007075:Immunoglobulin M / Q000276:immunology*; D016393:Lymphoma, B-Cell; D010716:Phosphatidylinositols / Q000378:metabolism; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D015398:Signal Transduction / Q000276:immunology; D014157:Transcription Factors / Q000235:genetics; D014407:Tumor Cells, Cultured
chemical_list: D000911:Antibodies, Monoclonal; D004268:DNA-Binding Proteins; C497325:EGR1 protein, human; D051766:Early Growth Response Protein 1; C486109:Egr1 protein, mouse; D006681:HLA-D Antigens; D017874:Immediate-Early Proteins; D007075:Immunoglobulin M; D010716:Phosphatidylinositols; D012333:RNA, Messenger; D014157:Transcription Factors; D011505:Protein-Tyrosine Kinases; D002118:Calcium