Lipopolysaccharide‐stimulated events in B Cell Activation

Publisher Website
Google Scholar
Abstract
High concentrations of thymus‐independent (T1) antigens are capable of inducing polyclonal B cell activation by their intrinsic mitogenic properties, irrespective of the specificity of the Ig receptors. Due to a genetic defect on the 4th chromosome, B cells from C3H/HeJ mice do not respond to lipopoly‐saccharide (LPS). In order to define at which step the mutation affects the signalling pathway, we compared B cells from C3H/HeJ and CBA mice with regard to changes of three events, namely cell size, and MHC class I and II antigen expression after LPS stimulation. We found that cell size and expression of MHC antigens increase in B cells from CBA mice after LPS stimulation, whereas B cells from C3H/HeJ mice do not respond at all. This suggests that the defect in C3H/HeJ mice interferes with early events in the signalling pathway, either due to the absence of a LPS receptor on B cell surface or the lack of an initial component necessary for effective signal transmission subsequent to LPS receptor binding. Our results also have shown that stimulation of anti‐Ig antibodies and LPS differ in some signalling events and have different final effects on B cells, which suggests that they may function differently via distinct signalling pathways.