Interleukin-10 induces immunoglobulin G isotype switch recombination in human CD40-activated naive B lymphocytes.

Malisan, Florence; Brière, Francine; Bridon, Jean-Michel; Harindranath, Nagaradona; Mills, Frederick C.; Max, Edward E.; Banchereau, Jacques; Martinez‐Valdez, Héctor

doi:10.1084/jem.183.3.937

Cited by 159 publications

(94 citation statements)

References 41 publications

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“…34,35 IL-10, together with anti-CD40 mAb, has been found to enhance IgG1 and IgG3 isotypes. 36,37 In B7-H1-costimulated T cells, although there is both increased IL-10 release and CD40L up-regulation observed ( Figure 3 and 8), there is no significant elevation of IgG1 and IgG3 in mB7-H1Ig-treated mice (Figure 7). Therefore, there is no simple explanation for selective increase of IgG2a antibody by B7-H1 costimulation.…”

Section: B7-h1 and T-helper Cell Functions 1815mentioning

confidence: 91%

B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function

Tamura

Dong

Zhu

et al. 2001

Blood

197

138

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B7-H1 is a recently described B7-like molecule that costimulates T-cell growth and cytokine secretion without binding to CD28, cytotoxic T-lymphocyte antigen-4 (CTLA-4), and inducible costimulator (ICOS). In this report, a mouse homologue of human B7-H1 is identified, and its immunologic functions are studied in vitro and in vivo. Mouse B7-H1 shares 69% amino acid homology to the human counterpart. Similar to human B7-H1, mouse B7-H1 can be induced to express on macrophages, T cells, and B cells and to enhance T-cell proliferation and secretion of interleukin-10 (IL-10), interferon-␥, and granulocyte-macrophage colony-stimulating factor but not IL-2 and IL-4. Furthermore, B7-H1 preferentially costimulates CD4 ؉ T cells independently of CD28 and enhances mixed lymphocyte responses to allogeneic antigens. In contrast to B7-1, expression of B7-H1 on murine P815 tumor cells by transfection fails to increase allogeneic and syngeneic cytolytic T-cell responses in vitro and in vivo. Administration of B7-H1Ig fusion protein, however, enhances keyhole limpet hemocyaninspecific T-cell proliferation and 2,4,6-trinitrophenyl-specific immunoglobulin G2a antibody production. The study thus identifies a unique costimulatory pathway that preferentially affects T-helper cell functions. IntroductionThe antigen-specific induction of proliferation and differentiation of lymphocytes requires a first signal delivered through T-cell or B-cell receptor together with a second, costimulatory signal. Stimulation of T cells by antigen in the absence of costimulation can result in unproductive T-cell responses or T-cell anergy. Engagement of CD28 by its natural ligand B7-1 or B7-2 promotes T-cell activation, proliferation, and the differentiation of effector functions for both CD4 ϩ and CD8 ϩ T cells. 1-3 CD28 triggering augments both Th1 and Th2 cytokine secretion including interleukin-2 (IL-2), interferon-␥ (IFN-␥), granulocytemacrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-␣ (TNF-␣), IL-4, IL-5, and IL-6 2,4 and up-regulates bcl-x L expression, which promotes T-cell survival. 5 Expression of B7-1 or B7-2 by tumor cells can enhance CD8 ϩ cytotoxic T lymphocyte (CTL) generation and differentiation in vitro and in vivo. [6][7][8][9][10] CTLA-4, the second receptor for B7-1 and B7-2, is believed to inhibit T-cell activation and IL-2 production by delivering an inhibitory signal. 11 Recently, several new B7-like molecules have been described to costimulate T-cell growth and cytokine production by binding to receptors other than CD28 and CTLA-4. Human and mouse B7h/B7RP-1 (GL50/LICOS/B7-H2) interact with an inducible receptor, ICOS, on T cells to costimulate T-cell growth in vitro. [12][13][14][15][16][17][18] More importantly, mice treated with B7RP-1 fusion protein had enhanced experimental contact hypersensitivity, and overexpression of soluble B7RP-1 in transgenic mice showed hyperplasia on several secondary lymphoid organs. 13 Taken together, these data suggest that the interaction between B7h/B7RP-1 and ICOS regulat...

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Section: B7-h1 and T-helper Cell Functions 1815mentioning

confidence: 91%

B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function

Tamura

Dong

Zhu

et al. 2001

Blood

197

138

View full text Add to dashboard Cite

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“…1). The IL-10/ IL-10R complex is a potent pathway for proliferation and maturation of B cells [14], as well a switch factor for IgG1 and IgG3 [15] and also enhances the survival of mature B lymphocytes according to the activation state of these cells [16]. Our results revealed a significant up-regulation of IL-10R expression by CD19 + cells at day 15 in parallel with the higher frequency of activated CD69 + B lymphocytes consistent the increased level of immunoglobulin observed 1-2 weeks following 17DD YF vaccination [3].…”

Section: Discussionmentioning

confidence: 99%

Activation/modulation of adaptive immunity emerges simultaneously after 17DD yellow fever first-time vaccination: is this the key to prevent severe adverse reactions following immunization?

Martins

Silva

Marciano

et al. 2007

Clinical and Experimental Immunology

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SummaryOver past decades the 17DD yellow fever vaccine has proved to be effective in controlling yellow fever and promises to be a vaccine vector for other diseases, but the cellular and molecular mechanisms by which it elicits such broadbased immunity are still unclear. In this study we describe a detailed phenotypic investigation of major and minor peripheral blood lymphocyte subpopulations aimed at characterizing the kinetics of the adaptive immune response following primary 17DD vaccination. Our major finding is a decreased frequency of circulating CD19+ cells at day 7 followed by emerging activation/modulation phenotypic features (CD19 + and CD8 + cells further support this hypothesis. We hypothesize that this controlled microenviroment seems to be the key to prevent the development of serious adverse events, and even deaths, associated with the 17DD vaccine reported in the literature.

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“…Among cytokines, IL-4 induces switching to IgG and IgE (66 -69), IL-10 to IgG and IgA (13,66,70,71), and TGF-␤ to IgA (71)(72)(73). In EBV-infected LMP1-expressing B cells, CSR to C ␥ and C ␣ occurs in the absence of exogenous cytokines.…”

Section: Discussionmentioning

confidence: 99%

EBV-Encoded Latent Membrane Protein 1 Cooperates with BAFF/BLyS and APRIL to Induce T Cell-Independent Ig Heavy Chain Class Switching

Raab‐Traub

Casali

et al. 2003

The Journal of Immunology

222

192

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By substituting the H chain C region of IgM with that of IgG, IgA, or IgE, class switching enables Abs to acquire new effector functions that are crucial for the neutralization of invading pathogens. Class switching occurs through class switch DNA recombination (CSR) and usually requires engagement of CD40 on B cells by CD40 ligand on Ag-activated CD4+ T cells. CSR must be tightly regulated because abnormal IgG and IgA production favors the onset of autoimmunity, whereas increased switching to IgE leads to atopy. These inflammatory disorders can be triggered or exacerbated by EBV infection. In this study, we show that EBV induces CD40-independent CSR from Cμ to multiple downstream Cγ, Cα, and Cε genes through latent membrane protein 1 (LMP1), a CD40-like viral protein that signals in a ligand-independent fashion. LMP1-induced CSR is associated with transcriptional activation of germline Cγ, Cα, and Cε genes and triggers the up-regulation of activation-induced cytidine deaminase, a crucial component of the CSR machinery. In addition, LMP1 induces B cells to express B cell-activating factor of the TNF family and a proliferation-inducing ligand, two molecules that mediate B cell survival and T cell-independent Ab production. B cell-activating factor of the TNF family and a proliferation-inducing ligand cooperate with LMP1 to induce Ig class switching because their neutralization by appropriate soluble decoy receptors attenuates CSR in LMP1-expressing B cells. By showing that LMP1 triggers T cell-independent CSR, our findings suggest that EBV could play an important role in the pathogenesis of disorders with aberrant IgG, IgA, and/or IgE production.

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Interleukin-10 induces immunoglobulin G isotype switch recombination in human CD40-activated naive B lymphocytes.

Cited by 159 publications

References 41 publications

B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function

B7-H1 costimulation preferentially enhances CD28-independent T-helper cell function

Activation/modulation of adaptive immunity emerges simultaneously after 17DD yellow fever first-time vaccination: is this the key to prevent severe adverse reactions following immunization?

EBV-Encoded Latent Membrane Protein 1 Cooperates with BAFF/BLyS and APRIL to Induce T Cell-Independent Ig Heavy Chain Class Switching

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