The lipid A moiety of lipopolysaccharide is specifically bound to B cell subpopulations of responder and nonresponder animals.

Employing autoradiography to detect [125I]-lipid A binding splenocytes and immunofluorescence to identify splenic B cells, it was observed that only a subpopulation of B cells bound lipid A. In contrast, non-B cells, including T cells and macrophage cells, exhibited either relatively little or no lipid A binding. LPS-responder and LPS-nonresponder substrains of mice exhibited essentially the same distribution of bound [125I]-lipid A among B cell subpopulations. Approximately 25% of the B splenocytes obtained from the LPS-responsive C3H/HeN substrain or from the LPS-nonresponsive C3H/HeJ, C57BL/10ScCR and C57BL/10ScN substrains bound [125I]-lipid A. On the other hand, 60% of the B splenocytes from both high- and low-responder mice derived from the CBA strain exhibited [125I]-lipid A binding. Taken in conjunction with the findings of other workers, these results are consistent with the possibility that the genetic defect in nonresponder mice is related to a lipid A triggering event rather than to lipid A binding.