An Intrinsic Propensity of Murine Peritoneal B1b Cells to Switch to IgA in Presence of TGF-β and Retinoic Acid

Roy, Bishnudeo; Brennecke, Anne-Margarete; Agarwal, Shiwani; Krey, Martina; Düber, Sandra; Weiß, Siegfried

doi:10.1371/journal.pone.0082121

Cited by 41 publications

(50 citation statements)

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“…However, we found no differences in IgE + B cells of Lgals3 +/+ and Lgals3 −/− mice (data not shown). As peritoneal B cells are committed to an IgA repertoire (Roy et al 2013) and as high levels of IgA are found in the serum during schistosomiasis (Gaber et al 2010), we monitored sIgA expression by peritoneal B cells and conclude that a significant correlation exists between galectin-3 and IgA + differentiating plasma cells in the peritoneal cavity. Kracker and colleagues demonstrated that IgA/IgM co-expression is a remarkable event in the course of immunoglobulin class switching (Kracker and Durandy 2011) and our data indicate that galectin-3 is a potent regulator of IgA expression on B1 cells during chronic schistosomiasis and cytokine induction.…”

Section: Discussionmentioning

confidence: 99%

“…*P<0.05 Peritoneal B1 lymphocytes express IL-5R constitutively (Hitoshi et al 1990) and higher levels of IL-5 in Lgals3 −/− mice (Oliveira et al 2009) and promptly synthesize IgA (Takatsu et al 2009). On the other hand, peritoneal B1 cells switch more readily to IgA than do splenic follicular or peritoneal B2 cells after B lymphocyte stimulator/lipopolysaccharide/TGF-β in vitro (Kaminski and Stavnezer 2006) and specifically, peritoneal B1b cells switch to IgA under the influence of the synergistic effect of TGF-β and retinoic acid (Roy et al 2013). Indeed, we have arguments to suggest that galectin-3 plays a regulatory role on IgA + cell differentiation controlling IL-5 and TGF-β functions in the peritoneal cavity.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, we evaluated whether the absence of galectin-3 interferes with Ig expression on peritoneal B cell subpopulations during the chronic phase of the disease. As B1 cells in mucosa-associated tissues are an important source of IgA-producing cells (Bao et al 1998;Roy et al 2013), we monitored the expression of surface IgA (sIgA) and IgM (sIgM) on peritoneal B1 cells in our model of infection. We observed that peritoneal B1a lymphocytes from Lgals3 −/− infected mice expressed lower levels of sIgM (Fig.…”

Section: Galectin-3 Inhibits Differentiation Of Peritoneal B1 Cells Imentioning

confidence: 99%

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

et al. 2015

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Galectin-3 is a β-galactoside-binding protein with an inhibitory role in B cell differentiation into plasma cells in distinct lymphoid tissues. We use a model of chronic schistosomiasis, a well-characterized experimental disease hallmarked by polyclonal B cell activation, in order to investigate the role of galectin-3 in controlling IgA production through peritoneal B1 cells. Chronically infected, galectin-3-deficient mice (Lgals3 −/− ) display peritoneal fluid hypercellularity, increased numbers of atypical peritoneal IgM + /IgA + B1a and B1b lymphocytes and histological disturbances in plasma cell niches when compared with Lgals3 + / + mice. Similar to our infection model, peritoneal B1 cells from uninfected Lgals3 −/− mice show enhanced switching to IgA after in vitro treatment with interleukin-5 plus transforming growth factor-β (IL-5 + TGF-β1). A higher number of IgA + B1a lymphocytes was found in the peritoneal cavity of Lgals3 −/− -uninfected mice at 1 week after i.p. injection of IL-5 + TGF-β1; this correlates with the increased levels of secreted IgA detected in the peritoneal fluid of these mice after cytokine treatment. Interestingly, a higher number of degranulated mast cells is present in the peritoneal cavity of uninfected and Schistosoma mansoni-infected Lgals3 −/− mice, indicating that, at least in part, mast cells account for the enhanced differentiation of B1 into IgAproducing B cells found in the absence of galectin-3. Thus, a novel role is revealed for galectin-3 in controlling the expression of surface IgA by peritoneal B1 lymphocytes; this might have important implications for manipulating the mucosal immune response.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Galectin-3 Inhibits Differentiation Of Peritoneal B1 Cells Imentioning

confidence: 99%

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

et al. 2015

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“…Another limitation of our study is that the population of B1a cells has been measured in peripheral blood and not in the intestinal mucosa. However, Roy et al [43] observed a considerable high propensity of murine splenic B1a cells to switch to IgA.…”

Section: Discussionmentioning

confidence: 99%

B1a Lymphocytes (CD19+CD5+) Deficiency in Patients with Crohn’s Disease and Its Relation with Disease Severity

Gil-Borrás

García‐Ballesteros

Benet-Campos

et al. 2018

Dig Dis

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Background/Aims: B1a cells (CD19+CD5+) are considered elements of the innate immune system. The aim of this study was to evaluate the frequency of B1a cells in the peripheral blood of patients with Crohn’s disease (CD) and its relation with disease severity. Methods: In this prospective study, a total of 128 subjects (64 CD patients and 64 healthy controls) were studied. B1a cells in peripheral blood, CD Activity Index, and Simple Endoscopic Score of B1a cells were studied. Results: A significant decrease of B1a cells in peripheral blood was observed in patients with CD versus controls (p = 0.002), especially in perforating or penetrating patterns (p = 0.017). A lower frequency of B1a cells is related to increased endoscopic severity (Spearman’s Rho: –0.559, p = 0.004). The mean frequency of B1a cells in patients with pre- and post-study surgery was significantly lower than that in patients who did not undergo surgery (p = 0.050 and p = 0.026, respectively). Conclusions: The B1a cell count in peripheral blood is lower in CD patients. This decrease is directly related to the severity of the disease (penetrating or perforating, Simple Endoscopy Score and surgery complication). These results pointed to the fact that B1a cells play an important role in immune protection in CD.

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“…In human B cells, RA increased IgA production and the expression of germ-line IgA1 and IgA2 transcripts (GLTa1 and GLTa2), and under the same conditions, RA did not increase IgM and IgG productions [41] . RA also plays a vital role together with TGF-β in the presence of Runx proteins on switching of different B cell subpopulations to IgA [42,43] . Yet no one focused on the role of RA in IgA CSR in IgAN.…”

Section: Discussionmentioning

confidence: 99%

Regulation of IgA Class Switch Recombination in Immunoglobulin A Nephropathy: Retinoic Acid Signaling and BATF

Peng²,

Chen³

et al. 2016

Am J Nephrol

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Background: Immunoglobulin (Ig) A nephropathy (IgAN) is the ﬁnding of immune deposits predominantly containing polymeric IgA in the glomerular mesangium on renal biopsy. Increasing evidence suggested that retinoic acid (RA) signaling selectively induces IgA isotype switching and basic leucine zipper transcription factor, ATF-like (BATF) controls the global regulators of class switch recombination (CSR) in lymphocytes. Great effort has been paid to identify whether impaired immune regulation along the ‘mucosa-bone marrow (BM) axis' play an important role in the pathogenesis of IgAN. Methods: The aim of the study was to investigate the expression of all-trans-RA (ATRA) and BATF, and to identify their impact on IgA CSR in IgAN patients and rat animal models. Blood samples and tonsillar tissue specimens were obtained from 22 patients with IgAN and 24 patients with chronic tonsillitis as control. Results: Immunohistochemical, RT-PCR and western blotting examination revealed that RA signaling and BATF productions are activated in IgAN patients compared with controls. Lipopolysaccharide and α-hemolytic streptococcus stimulation upregulated RA receptor (RAR) and BATF expression, promote IgA CSR and ATRA productions in tonsil mononuclear cells. RAR alpha (RARα) or BATF siRNA decreases IgA expression. We also built IgAN rat models and found that RARα, BATF and activation-induced cytidine deaminase were upregulated in the peripheral blood, spleen and BM. With ATRA (500 μg/kg body weight) treatment for 8 weeks, IgA deposition on glomeruli and mesangial cells proliferation increased. It also revealed that ATRA activated BATF and IgA CSR in vivo. Conclusion: These data point toward the role of RA signaling together with BATF in IgA CSR of IgAN, and the data also support the notion that mucosal immunization with neoantigen results in impaired mucosal and systemic IgA responses.

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An Intrinsic Propensity of Murine Peritoneal B1b Cells to Switch to IgA in Presence of TGF-β and Retinoic Acid

Cited by 41 publications

References 41 publications

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

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

B1a Lymphocytes (CD19+CD5+) Deficiency in Patients with Crohn’s Disease and Its Relation with Disease Severity

Regulation of IgA Class Switch Recombination in Immunoglobulin A Nephropathy: Retinoic Acid Signaling and BATF

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