Anti-immunoglobulin stimulation of murine lymphocytes. V. Age-related decline in Fc receptor-mediated immunoregulation
Scribner, D.J.; Weiner, H.L.; Moorhead, J.W.
Journal of Immunology 121(1): 377-382
1978
ISSN/ISBN: 0022-1767 PMID: 307581 Document Number: 133724
Anti-immunoglobulin (anti-Ig) antibodies can stimulate B -independent since anti-.theta. and complement treatment did not diminish responsiveness of B cells from aged mice. The lack of responsiveness of spleen cells from young mice is not due to suppressor T cells: T cell-depleted, B cell-enriched cultures of spleen cells from young mice remained unresponsive to anti-Ig; and responsiveness of B cells from aged mice was not suppressed by co-culture with spleen cells, purified splenic T cells or thymocytes from young mice. Additional experiments in which the stimulating ability of intact anti-Ig was compared to its Fab'2 counterpart (Fab'2 anti-Ig) revealed 2 significant findings. B cells from young mice that are normally unresponsive to intact anti-Ig responded well to Fab'2 anti-Ig. This response, measured at 72 h of culture, was profoundly inhibited by intact anti-Ig, even when the latter was added at 48 h. This indicates that active B cell proliferation can be inhibited by interactions of anti-Ig molecules with Fc receptors. B cells from aged mice responded significantly better to Fab'2 anti-Ig than to the intact molecule. However, addition of intact anti-Ig to these Fab'2-stimulated cultures resulted in relatively poor inhibition of the response. Apparently the ability of mouse B cells to respond to anti-Ig is related to the efficiency of Fc receptors in mediating inhibitory signals, the aging process in the mouse is accompanied by a decline in B cell regulation intrinsic to the B cell itself.