Switching capacity of FcϵRII‐positive and ‐negative murine B cells

Foy, Teresa M.; Waldschmidt, Thomas J.

doi:10.1002/eji.1830231225

Cited by 9 publications

(6 citation statements)

References 54 publications

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“…A significant difference between the response of splenic and peritoneal B cells to IL-5 has been reported (27)(28)(29). We observed simultaneous generation of B1-IgE + cells in the spleen and in the peritoneal cavity during the acute phase of the disease when the overall pattern of the immune response is Th2-dominated.…”

Section: Discussionsupporting

confidence: 58%

“…In vitro, the induction of IgE switch in B1 cells has been shown to be difficult, requiring very high levels of cytokines (29), in studies based on the production of IgM, IgG1, IgE, and IgA by B1 (CD23 -) and B2 lymphocytes (CD23 + ). Both subpopulations were obtained by sorting from the spleen and peritoneal cavity and cultured with lipopolysaccharide and IL-4.…”

Section: Discussionmentioning

confidence: 99%

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

Oliveira

Aguiar

Borojević

et al. 2005

Braz J Med Biol Res

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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.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

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

Oliveira

Aguiar

Borojević

et al. 2005

Braz J Med Biol Res

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“…The biological function of Thy1 is poorly understood, but it may likely be involved in signal transduction from the plasma membrane, because it was shown that thymocytes of Thy1-deficient mice exhibit augmented TCR signaling and impaired T cell differenti-ation (30). Other studies showed that LPS+IL-4-stimulated B cells, but not LPS-stimulated B cells, upregulate Thy1 (31,32). We confirm and extend these findings by showing that STAT6 expression in B cells is required for this effect.…”

Section: Discussionmentioning

confidence: 99%

Identification of Novel STAT6-Regulated Proteins in Mouse B Cells by Comparative Transcriptome and Proteome Analysis

Mokada-Gopal

Boeser

Lehmann

et al. 2017

The Journal of Immunology

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The transcription factor STAT6 plays a key role in mediating signaling downstream of the receptors for IL-4 and IL-13. In B cells, STAT6 is required for class switch recombination to IgE and for germinal center formation during type 2 immune responses directed against allergens or helminths. In this study, we compared the transcriptomes and proteomes of primary mouse B cells from wild-type and STAT6-deficient mice cultured for 4 d in the presence or absence of IL-4. Microarray analysis revealed that 214 mRNAs were upregulated and 149 were downregulated >3-fold by IL-4 in a STAT6-dependent manner. Across all samples, ∼5000 proteins were identified by label-free quantitative liquid chromatography/mass spectrometry. A total of 149 proteins was found to be differentially expressed >3-fold between IL-4–stimulated wild-type and STAT6−/− B cells (75 upregulated and 74 downregulated). Comparative analysis of the proteome and transcriptome revealed that expression of these proteins was mainly regulated at the transcriptional level, which argues against a major role for posttranscriptional mechanisms that modulate the STAT6-dependent proteome. Nine proteins were selected for confirmation by flow cytometry or Western blot. We show that CD30, CD79b, SLP-76, DEC205, IL-5Rα, STAT5, and Thy1 are induced by IL-4 in a STAT6-dependent manner. In contrast, Syk and Fc receptor–like 1 were downregulated. This dataset provides a framework for further functional analysis of newly identified IL-4–regulated proteins in B cells that may contribute to germinal center formation and IgE switching in type 2 immunity.

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“…Although the B220 ϩ CD23 Ϫ splenic subset contains immature as well as marginal zone B cells, the former is only a minor constituent of this population (7). BALB/c mice were used for isolating peritoneal B cell subsets because of the relatively high proportion of B1 B cells (10). Fig.…”

Section: Proliferative Response Of B Cell Subsets Stimulated With Rcd40lmentioning

confidence: 99%

“…Detailed studies by Rothstein and coworkers (11, 14 -16) have demonstrated B1 B cells to exhibit constitutively elevated levels of protein kinase C and nuclear activated STAT3, and to have decreased activation of phospholipase C-␥2 and NF-B after anti-IgM treatment. When assessing the ability of B1 and B2 B cells to differentiate and isotype switch upon culture with LPS plus cytokines, B2 B cells were found to produce high levels of IgM, IgG, and IgE, while B1 B cells secreted only high levels of IgM (5,10,17). The latter subset produced low levels of IgG and little or no IgE (5,10,17).…”

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confidence: 99%

Murine B1 B Cells Require IL-5 for Optimal T Cell-Dependent Activation

Erickson

Foy

Waldschmidt

2001

The Journal of Immunology

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T helper cell-driven activation of murine B cells has been shown to depend upon CD40-CD40 ligand (CD40L) interactions and a defined set of cytokines. These observations are primarily based on the use of conventional B cells obtained from the spleen. Therefore, it is presently unclear whether all mature B cell subsets found in the mouse have an equal dependence upon CD40-CD40L interactions and use the same T cell-derived cytokines. The present study tested the response of splenic follicular and marginal zone as well as peritoneal B2 and B1 B cells to Th cell stimulation. Splenic and peritoneal B cell subsets were sort purified based on CD23 expression, and cultured with rCD40L and cytokines or Th2 cells. The results demonstrate that follicular, marginal zone, and peritoneal B2 B cells require CD40-CD40L interactions and preferentially use IL-4 for optimal proliferation, differentiation, and isotype switching. In contrast, peritoneal B1 B cells use IL-5 in conjunction with CD40-CD40L interactions for maximal Th cell-dependent responses. Furthermore, B1 B cells are capable of proliferating, differentiating, and isotype switching in the absence of CD40-CD40L interactions. B1 B cells are able to respond to Th2 clones in the presence of anti-CD40L mAb as well as to Th2 clones derived from CD40L−/− mice. The CD40-CD40L-independent response of B1 B cells is attributable to the presence of both IL-4 and IL-5, and may explain the residual Ab response to T cell-dependent Ags in CD40L- or CD40-deficient mice, and in X-linked hyper-IgM (X-HIM) patients.

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Switching capacity of FcϵRII‐positive and ‐negative murine B cells

Cited by 9 publications

References 54 publications

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

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

Identification of Novel STAT6-Regulated Proteins in Mouse B Cells by Comparative Transcriptome and Proteome Analysis

Murine B1 B Cells Require IL-5 for Optimal T Cell-Dependent Activation

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