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Mechanisms involved in the inhibition of growth of a human B lymphoma cell line, B104, by anti-MHC class II antibodies.
- Source :
- Immunology & Cell Biology; Jun1994, Vol. 72 Issue 3, p205-214, 10p
- Publication Year :
- 1994
-
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 Ca<superscript>2+</superscript> concentration [Ca<superscript>2+</superscript>]<subscript>i</subscript> from the intracellular pool and little or no protein tyrosine phosphorylation, phosphatidyl inositol turnover, or expression of Egr-I mRNA, whereas 2.06 plus GAM induced an increase in [Ca<superscript>2+</superscript>]<subscript>i</subscript> 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<superscript>2+</superscript> -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. [ABSTRACT FROM AUTHOR]
- Subjects :
- LYMPHOMAS
CELL lines
IMMUNOGLOBULINS
TYROSINE
PHOSPHORYLATION
CHEMICAL reactions
Subjects
Details
- Language :
- English
- ISSN :
- 08189641
- Volume :
- 72
- Issue :
- 3
- Database :
- Complementary Index
- Journal :
- Immunology & Cell Biology
- Publication Type :
- Academic Journal
- Accession number :
- 17788651
- Full Text :
- https://doi.org/10.1038/icb.1994.31