IgE expression on the surface of B1 and B2 lymphocytes in experimental murine schistosomiasis

Abstract

In a previous study we monitored the distribution and phenotype expression of B1 cells during the evolution of experimental murine schistosomiasis mansoni and we proposed that the B1 cells were heterogeneous: a fraction which originated in the spleen and followed the migratory pathway to mesenteric ganglia, while the other was the resident peritoneal B1-cell pool. In the present study, we have addressed the question of whether these two B1-lymphocyte populations are involved in the production of the late Ig isotype IgE, which is present in high levels in schistosomal infection. Lymphocyte expression of surface markers and immunoglobulins were monitored by immunofluorescence flow cytometry. Both in the spleen and mesenteric ganglia, the B1 and B2 cells were induced to switch from IgM to IgE in the early Th2-dominated phase of the disease, with an increase of IgE in its later phases. Conversely, peritoneal B1-IgM + switched to the remaining IgE + present in high numbers in the peritoneal cavity throughout the disease. We correlated the efficient induction of the expression of late Ig isotypes by B1 cells with high levels of inflammatory cytokines due to the intense host response to the presence of worms and their eggs in the abdominal cavity. In conclusion, B1 cells have a different switch behavior from IgM to IgE indicating that these cell sub-populations depend on the microenvironment.

B cells induced by Schistosoma japonicum infection display diverse regulatory phenotypes and modulate CD4+ T cell response

“…Velupillai et al [37] have reported that B-1a cell outgrowth depends on the mouse strain during S. mansoni infection, and at early and acute infection, the frequencies of PerC B-1a cells change differently among various strains of infected mice. Besides, the percentages of splenic B-1a cells increase in C3H/HeN mice during acute and chronic S. mansoni infection [37,39]. Here, we observed that the proportions of PerC and splenic B-1a cells remained relatively constant at three weeks of S. japonicum infection, whereas these proportions were significantly reduced during acute and chronic schistosomiasis.…”

Lack of galectin-3 up-regulates IgA expression by peritoneal B1 lymphocytes during B cell differentiation

“…Previously, we have shown that peritoneal B1 cells from S. mansoni-infected mice switch from an IgM class to an IgE class (Oliveira et al 2005) and that infected Lgals3 −/− mice present high levels of serum IgE during schistosomiasis (Oliveira et al 2007). However, we found no differences in IgE + B cells of Lgals3 +/+ and Lgals3 −/− mice (data not shown).…”

“…In addition, soluble schistosoma-antigens and increased circulating levels of cytokines continuously stimulate peritoneal B cells during schitosomiasis (Pinho et al 2005;Weinberg et al 1992). In particular, peritoneal B1 lymphocytes have been shown to switch from IgM to IgE during S. mansoni infection (Oliveira et al 2005).…”

B-1 cells in immunotoxicology: Mechanisms underlying their response to chemicals and particles

“…Moreover, B1CD plasma cells also release “induced antibodies” or “pathogen-specific antibodies” in response to infection. A fraction of migrated B-1 cells undergo affinity maturation, increasing their specificity to the antigen ( Chen et al, 2003 ; Alugupalli et al, 2004 ) and class-switch toward IgA ( Kroese et al, 1989 ; New et al, 2020 ), IgG ( Hirose et al, 1993 ; Chen et al, 2003 ) and IgE ( Oliveira et al, 2005 ; Ghosh et al, 2012 ). These induced antibodies represent new additions to the B-1 cell repertoire.…”