Infect Immun  1986 Jan;51(1):224-32 

Immunoresponses to Neisseria meningitidis epitopes: suppression of secondary
response to phosphorylcholine is carrier specific.

Faro J, Seoane R, Eiras A, Lareo I, Couceiro J, Regueiro BJ.

Results of our previous work have shown that Neisseria meningitidis serogroup B
M986 can induce a phosphorylcholine (PC)-specific plaque-forming cell
immunoresponse in mice. Also, a single injection of a relatively low dose of
meningococci in NBF1 female mice induced a priming time-dependent suppression on
subsequent meningococcus challenge. This suppression was not due to switching to
another class of immunoglobulin nor to the presence of a capsule on N.
meningitidis. In this study we show that suppression induced by meningococcus is
carrier specific. Furthermore, we offer evidence suggesting that the
structure(s) on meningococcus that trigger this suppression is heat labile and
different from the antigenic structure(s) recognized by the suppressed B cells.
In addition, we found that there is a gradual increase in antibody secretion
rates of N. meningitidis-induced anti-PC plaque-forming cells that correlates
with N. meningitidis priming time. Rather unexpected was the fact that
pretreatment of mice with PC-keyhole limpet hemocyanin (thymus-dependent
antigen) had a great influence on the subsequent PC-specific immunoresponses
induced by N. meningitidis and PC-coupled heat-inactivated meningococcus
[PC-(NMB)HI], as shown by (i) a striking decrease in T15 idiotype expression,
(ii) concomitant direct anti-PC plaque-forming cells reduction, (iii) switching
to immunoglobulin G (N. meningitidis-induced immunoresponse) or immunoglobulin G
plus immunoglobulin A [PC-(NMB)HI-induced immunoresponse], and (iv) a
significant increase in heterogeneity of plaque-forming cell secretion rates.
The possibility that N. meningitidis, PC-(NMB)HI, and PC-KLH stimulate B
lymphocytes pertaining to three different subpopulations embedded in distinct
regulatory circuits is discussed, with emphasis on the interrelationships
between T-dependent and T-independent lymphocyte compartments. We focus on the
possibility of the existence of high-level regulatory circuits in which
lymphocyte subpopulations or sets of lymphocyte subpopulations with different
requirements of activation are connected.