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Serum factors and the cellular redox status regulate cellular responsiveness to MHC class II-triggered homotypic B
Cross-linking the major histocompatibility complex (MHC) class II (MHC-II) by their cognate ligands including mAb induces homotypic cell adhesion. It has been shown that merely surface MHC-II expression is insufficient to induce the response. We found that MHC-II-triggered cell adhesion in human B cell lines was absent when serum was removed from medium. Even in the presence of serum, the response was prevented when cells were treated with the glutathione synthesis inhibitor, buthionine sulfoximine, an irreversible catalase inhibitor, aminotriazole, and H2O2. Flow cytometrical analysis showed that these changes in cellular responsiveness were unlikely to be merely the result of altered surface Ag expression. In addition, the response was independent of the two major lymphocyte adhesion receptors, LFA-1 and intercellular adhesion molecule-1 (ICAM-1). These findings suggest that serum- and redox-sensitive intracellular events regulate cellular responsiveness to MHC-II-triggered LFA-1/ICAM-1-independent cell adhesion independently of differentiation.
Cross-linking the major histocompatibility complex (MHC) class II (MHC-II) by their cognate ligands including mAb induces homotypic cell adhesion. It has been shown that merely surface MHC-II expression is insufficient to induce the response. We found that MHC-II-triggered cell adhesion in human B cell lines was absent when serum was removed from medium. Even in the presence of serum, the response was prevented when cells were treated with the glutathione synthesis inhibitor, buthionine sulfoximine, an irreversible catalase inhibitor, aminotriazole, and H2O2. Flow cytometrical analysis showed that these changes in cellular responsiveness were unlikely to be merely the result of altered surface Ag expression. In addition, the response was independent of the two major lymphocyte adhesion receptors, LFA-1 and intercellular adhesion molecule-1 (ICAM-1). These findings suggest that serum- and redox-sensitive intracellular events regulate cellular responsiveness to MHC-II-triggered LFA-1/ICAM-1-independent cell adhesion independently of differentiation.