Regulatory B cells in CVID patients fail to suppress multifunctional IFN-gamma+TNF-alpha(+)CD4(+) T cells differentiation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F15%3A10315974" target="_blank" >RIV/00216208:11130/15:10315974 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/15:00084180 RIV/00159816:_____/15:00063571 RIV/00064203:_____/15:10315974

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.clim.2015.06.013" target="_blank" >http://dx.doi.org/10.1016/j.clim.2015.06.013</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.clim.2015.06.013" target="_blank" >10.1016/j.clim.2015.06.013</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Regulatory B cells in CVID patients fail to suppress multifunctional IFN-gamma+TNF-alpha(+)CD4(+) T cells differentiation

Popis výsledku v původním jazyce

Common variable immunodeficiency (CVID) refers to primary hypogammaglobulinemia with unknown pathogenesis. Although there is evidence for intrinsic B cell defects in some CVID patient groups, various abnormalities in cytokine production by T cells in CVID patients are frequently observed. Here, we demonstrate a relationship in the production of pro-inflammatory Th1 cytokines and regulatory B cells producing IL-10 between CVID patients and healthy controls. We describe CD19(+)CD24(hi)CD38(hi)IL-10(+) regulatory B cells generated after T cell stimulation of human peripheral blood lymphocytes ex vivo are able to suppress IFN-gamma+TNF-alpha(+) producing CD4(+) T cells. This process is impaired in CVID patients, who present with both low numbers of CD19(+)CD24(hi)CD38(hi)IL-10(+) B cells and increased numbers of IFN-gamma+TNF-alpha(+)CD4(+) T cells. Disruption of the regulatory B cell response to T cell stimulation explains the excessive T cell activation regarded as an immunoregulatory abnormality that is a frequent finding in CVID patients.

Název v anglickém jazyce

Regulatory B cells in CVID patients fail to suppress multifunctional IFN-gamma+TNF-alpha(+)CD4(+) T cells differentiation

Popis výsledku anglicky

Common variable immunodeficiency (CVID) refers to primary hypogammaglobulinemia with unknown pathogenesis. Although there is evidence for intrinsic B cell defects in some CVID patient groups, various abnormalities in cytokine production by T cells in CVID patients are frequently observed. Here, we demonstrate a relationship in the production of pro-inflammatory Th1 cytokines and regulatory B cells producing IL-10 between CVID patients and healthy controls. We describe CD19(+)CD24(hi)CD38(hi)IL-10(+) regulatory B cells generated after T cell stimulation of human peripheral blood lymphocytes ex vivo are able to suppress IFN-gamma+TNF-alpha(+) producing CD4(+) T cells. This process is impaired in CVID patients, who present with both low numbers of CD19(+)CD24(hi)CD38(hi)IL-10(+) B cells and increased numbers of IFN-gamma+TNF-alpha(+)CD4(+) T cells. Disruption of the regulatory B cell response to T cell stimulation explains the excessive T cell activation regarded as an immunoregulatory abnormality that is a frequent finding in CVID patients.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EC - Imunologie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical Immunology

ISSN

1521-6616

e-ISSN

—

Svazek periodika

160

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

9

Strana od-do

292-300

Kód UT WoS článku

000362151500019

EID výsledku v databázi Scopus

2-s2.0-84938249215