Detailed Information on Publication Record
2021
TNFR2 expression is a hallmark of human memory B cells with suppressive function
TICHA, Olga, Peter SLANINA, Lukas MOOS, Julie ŠTÍCHOVÁ, Marcela VLKOVÁ et. al.Basic information
Original name
TNFR2 expression is a hallmark of human memory B cells with suppressive function
Authors
TICHA, Olga (203 Czech Republic), Peter SLANINA (703 Slovakia, belonging to the institution), Lukas MOOS, Julie ŠTÍCHOVÁ (203 Czech Republic, belonging to the institution), Marcela VLKOVÁ (203 Czech Republic, belonging to the institution) and Isabelle BEKEREDJIAN-DING (guarantor)
Edition
EUROPEAN JOURNAL OF IMMUNOLOGY, HOBOKEN, WILEY, 2021, 0014-2980
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30102 Immunology
Country of publisher
United States of America
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 6.688
RIV identification code
RIV/00216224:14110/21:00121608
Organization unit
Faculty of Medicine
UT WoS
000626550800001
Keywords in English
B cells; Breg; IL‐ 10; TLR9; TNFR2
Tags
International impact, Reviewed
Změněno: 7/12/2021 13:44, Mgr. Tereza Miškechová
Abstract
V originále
Tumor Necrosis Factor Receptor 2 (TNFR2) expression is increasingly being linked to tolerogenic immune reactions and cells with suppressor function including a subset of T-regulatory cells. B-regulatory cells play an important role in control of T-cell responses and inflammation. Recently, we described TNFR2 as a marker for IL-10-producing B cells, a hallmark of this cell subset. Here, we demonstrate that proliferation of T cells is reduced in the presence of TNFR2 positive human memory B cells generated with TLR9 ligand, while TNFR2- and TNFR2+CD27- B cells display costimulatory activity. Our data further reveal that IL-10 secretion is characteristic of IgM+ naive and memory B cells but suppressive activity is not restricted to IL-10: (i) the inhibitory effect of TNFR2+ switched memory B cells was comparable to that exerted by TNFR2+ IgM+ memory B cells although IL-10 secretion levels in the cocultures were lower; (ii) supernatants from TNFR2+ memory B cells failed to suppress T-cell proliferation. Based on our findings, we propose that formation of Breg is a specific characteristic of human memory B cells undergoing terminal differentiation. Our data further corroborate that TNFR2 represents a viable marker for identification of memory B cells with regulatory function.