High concentrations of thymus-independent (TI) antigens are capable of
inducing polyclonal B cell activation by their intrinsic mitogenic pr
operties, irrespective of the specificity of the Ig receptors. Due to
a genetic defect on the 4th chromosome, B cells from C3H/HeJ mice do n
ot respond to lipopolysaccharide (LPS). In order to define at which st
ep the mutation affects the signalling pathway, we compared B cells fr
om 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 stimul
ation. 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 C
3H/HeJ mice interferes with early events in the signalling pathway, ei
ther due to the absence of a LPS receptor on B cell surface or the lac
k of an initial component necessary for effective signal transmission
subsequent to LPS receptor binding. Our results also have shown that s
timulation of anti-Ig antibodies and LPS differ in some signalling eve
nts and have different final effects on B cells, which suggests that t
hey may function differently via distinct signalling pathways.