Cross Talk between Peritoneal Macrophages and B-1 Cells In Vitro

Abstract

B-1 cells constitute a distinct B cell population with unique phenotypic and functional characteristics. They represent the main B cell population found in mouse peritoneal and pleural cavities. The communication between B-1 cells and peritoneal macrophages has been previously studied, and the effect this interaction has on macrophages has been previously described. Using an in vitro co-culture model, herein we demonstrated that peritoneal macrophages were able to increase survival rates and to stimulate proliferation of B-1 cells. IL-6 was also found to be important in B-1 cell survival; recombinant IL-6 increases the percentage of viable B-1 cells in culture. Furthermore, molecules involved in the IL-6 signaling pathway, such as STAT-3 and Bcl-2, were highly expressed in B-1 cells after co-culture with peritoneal macrophages. IL-6-deficient peritoneal macrophages were not able to increase B-1 cell survival, confirming the importance of this cytokine. Altogether, our results indicate a novel mechanism in which peritoneal macrophages are able to regulate the B-1 population via IL-6 secretion.

B-1a cells protect mice from sepsis-induced acute lung injury

“…The crosstalk effect between B-1a cells and macrophages has been demonstrated in previous reports (Thies et al 2013 ; Barbeiro et al 2011 ). B-1a cells produce IL-10 in response to LPS stimulation (Aziz et al 2017 ; Barbeiro et al 2011 ).…”

S1P 2 /G 12/13 Signaling Negatively Regulates Macrophage Activation and Indirectly Shapes the Atheroprotective B1-Cell Population

“…Coculture experiments between wild-type B1 cells and control or Gα 12/13 -deficient rpMP showed that B1 viability was increased in the presence of mutant rpMP, indicating that the preactivated state of these cells directly contributes to the augmentation of the B1 population ( Figure 5F). IL-6, a cytokine that shows increased expression in Gα 12/13 -deficient rpMP, has been suggested to mediate increased B1-cell viability, 33 but we did not observe an effect of IL-6-blocking antibodies on B1 viability ( Figure 5F), indicating that enhanced IL-6 signaling alone cannot explain rpMP-induced increases in B1 viability.…”

“…This is in line with a recent report showing that peritoneal macrophages are able to increase survival and proliferation of B1 cells. 33 Although conventional B2 cells are considered to be atherogenic, 12 B1 cells and B1-derived natural IgM idiotypes have antiatherogenic effects because of their ability to scavenge oxLDL and to enhance clearing of apoptotic cells. [34][35][36] Whether the observed reduction of apoptotic cells in plaques of Lys-G 12/13 -KOs is because of enhanced T15/E06-mediated clearance or because of the generally reduced inflammatory reaction and plaque size is currently unknown.…”

Macrophage regulation of B cell proliferation

“…B10/B reg cells suppress pathogenic TH1 and TH17 cells and induce production of T regs [50]. Although B2 cells generally responded better than B1 cells under macrophage-dense conditions, this environment has the potential to promote B2 cell conversion into B1 cells, generating cells with enhanced survival capability [51, 52]. Considering the potent ability of IL-10 to temper cell-mediated immunity, this characteristic is perhaps most problematic for B cell activation in TMEs.…”