Immunoresponses to Neisseria meningitidis epitopes: Immunodulation by meningococcus B acts on more than one meningococcal surface epitope

Abstract

Neisseria meningitidis group B strain M986 (serotypes 2a, 7) (NMB) elicits a specific primary antiphosphorylcholine immune response in mice but not a secondary response. The ability of other serotype and serogroup meningococci to induce similar primary responses in mice was studied, as was the immunogenicity of trinitrophenyl coupled NMB (TNP-NMB) in primary and secondary antitrinitrophenyl responses. Except for NMB, all other strains tested (three serogroup B and one serogroup A meningococcal strains) were found to be very poor phosphorylcholine immunogens. TNP-NMB, however, though proving to be a very good TNP antigen, was only a weak phosphorylcholine antigen. Priming NBF1 female mice with TNP-NMB one month or more before challenging them with the same antigen induced a strong depression of anti-TNP response in the subsequent challenge. However, this effect was not observed with Xid NBF1 male mice. Furthermore, priming mice with NMB weakly affected the anti-TNP response, but greatly depressed the antiphosphorylcholine response, after TNP-NMB challenge. In addition, whereas apparently only one TNP-specific B cell subpopulation was responding in unprimed mice challenged simultaneously with TNP-NMB and TNP-Ficoll (non-additive response), priming mice with NMB appeared to facilitate the independent activation of two different TNP-specific B cell subpopulations (additive response).

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine

“…Although suppression might be due to an antibody-dependent mechanism [45], this would imply that the immune response to other PC antigens should also be suppressed in NMBprimed mice, and this is not the case [15]. Moreover, this suppression does not seem to be due either to anti-NMB antibodies or to the so-called epitope-specific suppression [23 ], because the suppression is detected only when the epitope is present in the carrier in both the priming and the challenge [16]. Therefore, a more likely explanation is that suppression is due to NMB-primed non-B, non-T radioresistant cells; of these, the best cell candidate appears to be macrophages or macrophage-like cells.…”

The Fine Structure of Neisseria meningitidis Lipooligosaccharide from the M986 Strain and Three of Its Variants

“…Inoculation of mice with outer membrane vesicles from both encapsulated and non-encapsulated M986 strains has been shown to provide protection against lethal doses of endotoxin and infective doses of live bacteria (19). These strains have also been used to investigate immune regulatory properties of N. meningitidis (26,27) and both LOS and outer membrane vesicles enhance granulocyte recovery in myelosuppressed mice (22).…”

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

“…Some antigenic preparations of N. meningitidis can induce a phosphorylcholine-specific response acting as a type 2 T-independent antigen (7) and can modulate this immunoresponse by causing carrier-specific suppression of the secondary response against natural and chemically bound meningococcal epitopes (7)(8)(9).…”

“…Neisseria meningitidis group B as much other Gramnegative bacteria is a complex and particulate antigen able to elicit multiple immunomodulatory mechanisms at both molecular and cellular immunological level such as secretion of IgA proteases (22). Some antigenic preparations of N. meningitidis can induce a phosphorylcholine-specific response acting as a type 2 T-independent antigen (7) and can modulate this immunoresponse by causing carrier-specific suppression of the secondary response against natural and chemically bound meningococcal epitopes (7)(8)(9).…”