Interference between Neisseria meningitidis and PC‐KLH Induced Anti‐Phosphorylcholine PFC Responses in NZB/W Autoimmune Mice

Abstract

In this work, we demonstrate that the simultaneous injection of PC-KLH and Neisseria meningitidis-derived antigens [NMB or PC-(NMB)HI] induced in old NZB/W mice defective responses as does PC-KLH challenge. On the other hand, the simultaneous injection of both immunogenic preparations of N. meningitidis evoked responses similar to those shown by old mice challenged with NMB alone. Alteration in PC-specific PFC responses also affected hapten-free inhibition profiles and their heterogeneities. The increase in PC50s of anti-phosphorylcholine PFC responses and their heterogeneities induced by certain antigens with aging is correlated with a decrease in T15 idiotype expression, suggesting that after the T15 dominant clone disappears no other clone takes control of the anti-PC response. These results suggest that the mechanism(s) involved in the regulation of T15 marker expression play an important role in the inability of old NZB/W mice to mount good anti-PC responses and suggest that regulatory mechanisms induced by PC-KLH dominate those elicited by NMB.

Cross-reactivity of anti-phosphorylcholine antibodies to neuromuscular blockers in a murine model of immunization

“…The equivalent in humans is the IgG2 isotype, that presents an overwhelming response to PC, comprising more than 80% of all immunoglobulins [22,]. Phosphorylcholine is a component of several bacterial, mycotic and parasitic antigens [23][24][25] and antibodies induced by PC-KLH immunization in mice could mediate protection against Streptococcus pneumoniae and Neisseria meningitidis infections [26,27]. This isotype is also represented among natural anti-PC antibodies, as well as in antipneumococcal vaccinationinduced antibodies [22,28].…”