IFN-γ enhances secretion of IgG2a from IgG2a-committed LPS-stimulated murine B cells: Implications for the role of IFN-γ in class switching

Bossie, A; Vitetta, Ellen S.

doi:10.1016/0008-8749(91)90257-c

Cited by 95 publications

(69 citation statements)

References 14 publications

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“…To confirm the ELISA results that the supernatants from restimulated Th1 cells contained more IFN-␥, we measured the ability of these supernatants to increase the amount of IgG2a Ab produced by LPS-activated B cells (27). LPS-activated B cells produced significantly more IgG2a when exposed to supernatants from restimulated Th1 cells derived in the presence of NE when compared with B cells exposed to control supernatants (Fig.…”

Section: Ifn-␥ Production By Th1 Cells Generated From Naive T Cells Amentioning

confidence: 70%

IFN-γ Production by Th1 Cells Generated from Naive CD4+ T Cells Exposed to Norepinephrine

Swanson

Lee

Sanders

2001

The Journal of Immunology

180

117

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During activation in vivo, naive CD4+ T cells are exposed to various endogenous ligands, such as cytokines and the neurotransmitter norepinephrine (NE). To determine whether NE affects naive T cell differentiation, we used naive CD4+ T cells sort-purified from either BALB/c or DO11.10 TCR-transgenic mouse spleens and activated these cells with either anti-CD3/anti-CD28 mAbs or APC and OVA323–329 peptide, respectively, under Th1-promoting conditions. RT-PCR and functional assays using selective adrenergic receptor (AR) subtype antagonists showed that naive CD4+ T cells expressed only the β2AR subtype to bind NE and that stimulation of this receptor generated Th1 cells that produced 2- to 4-fold more IFN-γ. This increase was due to more IFN-γ produced per cell upon restimulation instead of more IFN-γ-secreting cells, as determined by IFN-γ-specific immunofluorescence and enzyme-linked immunospot. In contrast, Th1 cell differentiation was unaffected when naive T cells were exposed to NE and activated either in the presence of a neutralizing anti-IL-12 mAb or by APC from IL-12-deficient mice. Moreover, the addition of IL-12 to the IL-12-deficient APC cultures restored the ability of NE to increase Th1 differentiation. Taken together, these results indicate that a possible link may exist between the signaling pathways used by NE and IL-12 to increase naive CD4+ T cell differentiation to a Th1 cell.

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Section: Ifn-␥ Production By Th1 Cells Generated From Naive T Cells Amentioning

confidence: 70%

IFN-γ Production by Th1 Cells Generated from Naive CD4+ T Cells Exposed to Norepinephrine

Swanson

Lee

Sanders

2001

The Journal of Immunology

180

117

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“…In fact, IL-4 directs murine IgE and IgG1 production, whereas IFN-g stimulates selectively the production of IgG2a as well as that of IgG3 under certain circumstances [43,44]. Other studies have reported the association of IL-17 with IgG production in animals with autoimmune disease and the presence of low levels of anti-CII IgG2a antibodies in IL-17-deficient mice [8,45].…”

Section: T Cells or Other Cd4mentioning

confidence: 99%

Activation of natural killer T cells by α-carba-GalCer (RCAI-56), a novel synthetic glycolipid ligand, suppresses murine collagen-induced arthritis

Yoshiga

Goto

Segawa

et al. 2011

Clinical and Experimental Immunology

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SummaryAlpha-carba-GalCer (RCAI-56), a novel synthetic analogue of agalactosylceramide (a-GalCer), stimulates invariant natural killer T (NK T) cells to produce interferon (IFN)-g. IFN-g exhibits immunoregulatory properties in autoimmune diseases by suppressing T helper (Th)-17 cell differentiation and inducing regulatory T cells and apoptosis of autoreactive T cells. Here, we investigated the protective effects of a-carba-GalCer on collageninduced arthritis (CIA) in mice. First, we confirmed that a-carba-GalCer selectively induced IFN-g in CIA-susceptible DBA/1 mice in vivo. Then, DBA/1 mice were immunized with bovine type II collagen (CII) and a-carbaGalCer. The incidence and clinical score of CIA were significantly lower in a-carba-GalCer-treated mice. Anti-IFN-g antibodies abolished the beneficial effects of a-carba-GalCer, suggesting that a-carba-GalCer ameliorated CIA in an IFN-g-dependent manner. Treatment with a-carba-GalCer reduced anti- Th17 ratio). Moreover, the gene expression levels of IL-6 and IL-23p19, Th17-related cytokines, were reduced significantly in mice treated with a-carba-GalCer. In addition, we observed higher IFN-g production by NK T cells in a-carba-GalCer-treated mice in the initial phase of CIA. These findings indicate that a-carba-GalCer polarizes the T cell response toward Th1 and suppresses Th17 differentiation or activation, suggesting that a-carbaGalCer, a novel NK T cell ligand, can potentially provide protection against Th17-mediated autoimmune arthritis by enhancing the Th1 response. CII antibody production [immunoglobulin (Ig)G and IgG2a] and CIIreactive interleukin (IL)-17 production by draining lymph node (DLN) cells, did not induce apoptosis or regulatory T cells, and significantly increased the ratio of the percentage of IFN-g-producing T cells to IL-17-producing T cells (Th1/

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“…␥2b H chains are induced in tissue culture by LPS, and are enhanced further by treatment with TGF␤ (3,4). Expression of the murine ␥2a gene in vitro is induced only weakly by LPS, but robustly by LPS ϩ IFN-␥ (5,6). In vivo and in vitro, induction of the ␥2a gene by T cell-independent Ags depends on the transcription factor T-bet (7,8).…”

Section: Induced Expression Of Murinementioning

confidence: 99%

“…In vivo and in vitro, induction of the ␥2a gene by T cell-independent Ags depends on the transcription factor T-bet (7,8). Although induction of the ␥2a H chain genes after B cell activation via a TLR (by LPS or CpG) has been investigated thoroughly (5,6,9), the induction of the ␥2a in the context of stimulation via T cell help (by CD40 ligation) has been relatively understudied (4). Induction of ␥2a to T cell-dependent Ags is independent of T-bet (8), implying that T cell-independent and T cell-dependent switch recombination to ␥2a differ.…”

Section: Induced Expression Of Murinementioning

confidence: 99%

Induced Expression of Murine γ2a by CD40 Ligation Independently of IFN-γ

Collins

Shi

Burrell

et al. 2006

The Journal of Immunology

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IgG2a, with γ2a H chains, is important for protection against viruses and other intracellular pathogens. Although a large portion of IgG2a expression is dependent upon IFN-γ, some germline transcription and switch recombination to the murine γ2a H chain gene expression are independent of IFN-γ. We found that agonistic anti-CD40 Abs injected into IFN-γ-deficient mice induce a >200-fold increase in the amount of serum Ig2a, while other Ig isotypes are increased by 16-fold or less. In vitro, ligation of CD40 on B cells, without the addition of other B cell activators or cytokines, results in germline transcription and switch recombination that are largely restricted to the γ2a gene. These results suggest that some immune responses to infectious agents can result in large amounts of IgG2a expression through ligation of CD40, without the expression of IFN-γ by Th1 or other cells.

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IFN-γ enhances secretion of IgG2a from IgG2a-committed LPS-stimulated murine B cells: Implications for the role of IFN-γ in class switching

Cited by 95 publications

References 14 publications

IFN-γ Production by Th1 Cells Generated from Naive CD4+ T Cells Exposed to Norepinephrine

IFN-γ Production by Th1 Cells Generated from Naive CD4+ T Cells Exposed to Norepinephrine

Activation of natural killer T cells by α-carba-GalCer (RCAI-56), a novel synthetic glycolipid ligand, suppresses murine collagen-induced arthritis

Induced Expression of Murine γ2a by CD40 Ligation Independently of IFN-γ

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