MIP-1<i>α</i>Induces Differential MAP Kinase Activation and I<i>κ</i>B Gene Expression in Human B Lymphocytes

Teague, Ryan M.; Harlan, Lisa M.; Benedict, Stephen H.; Chan, Marcia A.

doi:10.1089/1079990041535656

Cited by 6 publications

(4 citation statements)

References 41 publications

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“…We propose that the presence of a small but highly active population of polyfunctional B cells in HHV-8 infection has detrimental rather than beneficial outcomes. HHV-8-infected B cells produced elevated levels of MIP-1α and -β, which are chemokines involved in B cell recruitment, activation, and immunoglobulin production (38, 39). MIP-1α and -β could increase the activated B cell population most capable of replicating HHV-8.…”

Section: Discussionmentioning

confidence: 99%

Human Herpesvirus 8 Induces Polyfunctional B Lymphocytes That Drive Kaposi’s Sarcoma

Knowlton

Rappocciolo

Piazza

et al. 2014

mBio

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Kaposi’s sarcoma (KS) is an unusual neoplasia wherein the tumor consists primarily of endothelial cells infected with human herpesvirus 8 (HHV-8; Kaposi’s sarcoma-associated herpesvirus) that are not fully transformed but are instead driven to excess proliferation by inflammatory and angiogenic factors. This oncogenic process has been postulated but unproven to depend on a paracrine effect of an abnormal excess of host cytokines and chemokines produced by HHV-8-infected B lymphocytes. Using newly developed measures for intracellular detection of lytic cycle proteins and expression of cytokines and chemokines, we show that HHV-8 targets a range of naive B cell, IgM memory B cell, and plasma cell-like populations for infection and induction of interleukin-6, tumor necrosis factor alpha, macrophage inhibitory protein 1α, macrophage inhibitory protein 1β, and interleukin-8 in vitro and in the blood of HHV-8/HIV-1-coinfected subjects with KS. These B cell lineage subsets that support HHV-8 infection are highly polyfunctional, producing combinations of 2 to 5 of these cytokines and chemokines, with greater numbers in the blood of subjects with KS than in those without KS. Our study provides a new paradigm of B cell polyfunctionality and supports a key role for B cell-derived cytokines and chemokines produced during HHV-8 infection in the development of KS.

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Section: Discussionmentioning

confidence: 99%

Human Herpesvirus 8 Induces Polyfunctional B Lymphocytes That Drive Kaposi’s Sarcoma

Knowlton

Rappocciolo

Piazza

et al. 2014

mBio

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“…B cells were isolated from tonsillar tissue as we have routinely done and described [13]. Briefly, tonsillar tissue was teased apart and cells diluted in HBSS (Gibco/Invitrogen, Carlsbad, CA).…”

Section: Methodsmentioning

confidence: 99%

Omalizumab may decrease IgE synthesis by targeting membrane IgE+ human B cells

Chan

Gigliotti

Dotson

et al. 2013

Clinical & Translational All

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BackgroundOmalizumab, is a humanized anti-IgE monoclonal antibody used to treat allergic asthma. Decreased serum IgE levels, lower eosinophil and B cell counts have been noted as a result of treatment. In vitro studies and animal models support the hypothesis that omalizumab inhibits IgE synthesis by B cells and causes elimination of IgE-expressing cells either by induction of apoptosis or induction of anergy or tolerance.MethodsWe examined the influence of omalizumab on human tonsillar B cell survival and on the genes involved in IgE synthesis. Tonsillar B cells were stimulated with IL-4 plus anti-CD40 antibody to induce class switch recombination to IgE production in the presence or absence of omalizumab. Cell viability was assessed and RNA extracted to examine specific genes involved in IgE synthesis.ConclusionsWe found that omalizumab reduced viable cell numbers but this was not through induction of apoptosis. IL-4R and germline Cϵ mRNA levels were decreased as well as the number of membrane IgE+ cells in B cells treated with omalizumab. These data suggest that omalizumab may decrease IgE synthesis by human B cells by specifically targeting membrane IgE-bearing B cells and inducing a state of anergy.

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“…Furthermore, the accumulation of B cells in this organ might also explain the reduction previously observed in the spleen. Moreover, it was seen that ouabain inhibits p38 activation in T cells (Rodrigues-Mascarenhas et al, 2008) and it is involved in the MIP-1 signal transduction pathway that stimulates human B cell migration in vitro (Teague et al, 2004). Therefore, similarly to what occurs in T lymphocytes, the inactivation of p38 in B lymphocytes could also justify the retention of these cells in lymph nodes.…”

Section: Discussionmentioning

confidence: 97%

Dynamics of murine B lymphocytes is modulated by in vivo treatment with steroid ouabain

et al. 2016

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MIP-1αInduces Differential MAP Kinase Activation and IκB Gene Expression in Human B Lymphocytes

Cited by 6 publications

References 41 publications

Human Herpesvirus 8 Induces Polyfunctional B Lymphocytes That Drive Kaposi’s Sarcoma

Human Herpesvirus 8 Induces Polyfunctional B Lymphocytes That Drive Kaposi’s Sarcoma

Omalizumab may decrease IgE synthesis by targeting membrane IgE+ human B cells

Dynamics of murine B lymphocytes is modulated by in vivo treatment with steroid ouabain

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