scholarly journals Correction to: The immunomodulatory functions and molecular mechanism of a new bursal heptapeptide (BP7) in immune responses and immature B cells

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Xiu Li Feng ◽  
Yang Zheng ◽  
Man Man Zong ◽  
Shan Shan Hao ◽  
Guang Fang Zhou ◽  
...  
Keyword(s):  
B Cells ◽  
Immune Responses ◽  
Molecular Mechanism ◽  
Immature B Cells

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals Hepatitis C Virus Induces Toll-Like Receptor 4 Expression, Leading to Enhanced Production of Beta Interferon and Interleukin-6

2006 ◽  
Vol 80 (2) ◽  
pp. 866-874 ◽  
Author(s):  
Keigo Machida ◽  
Kevin T. H. Cheng ◽  
Vicky M.-H. Sung ◽  
Alexandra M. Levine ◽  
Steven Foung ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
B Cells ◽  
Immune Responses ◽  
Interleukin 6 ◽  
Innate Immune ◽  
Hcv Infection ◽  
Innate Immune Responses ◽  
Altered Expression ◽  
Beta Interferon

ABSTRACT Hepatitis C virus (HCV) induces inflammatory signals, leading to hepatitis, hepatocellular carcinomas, and lymphomas. The mechanism of HCV involvement in the host's innate immune responses has not been well characterized. In this study, we analyzed expression and regulation of the entire panel of toll-like receptors (TLRs) in human B cells following HCV infection in vitro. Among all of the TLRs (TLRs 1 to 10) examined, only TLR4 showed an altered expression (a three- to sevenfold up-regulation) after HCV infection. Peripheral blood mononuclear cells from HCV-infected individuals also showed a higher expression level of TLR4 compared with those of healthy individuals. HCV infection significantly increased beta interferon (IFN-β) and interleukin-6 (IL-6) secretion from B cells, particularly after lipopolysaccharide stimulation. The increased IFN-β and IL-6 production was mediated by TLR4 induction, since the introduction of the small interfering RNA against TLR4 specifically inhibited the HCV-induced cytokine production. Among all of the viral proteins, only NS5A caused TLR4 induction in hepatocytes and B cells. NS5A specifically activated the promoter of the TLR4 gene in both hepatocytes and B cells. In conclusion, HCV infection directly induces TLR4 expression and thereby activates B cells, which may contribute to the host's innate immune responses.

LSP1 regulates anti-IgM induced apoptosis in WEHI-231 cells and normal immature B-cells

1999 ◽  
Vol 36 (6) ◽  
pp. 349-359 ◽  
Author(s):  
J Jongstra-Bilen ◽  
A Wielowieyski ◽  
V Misener ◽  
J Jongstra
Keyword(s):  
B Cells ◽  
Wehi 231 ◽  
Immature B Cells ◽  
Induced Apoptosis

Increased Apoptosis of CD20+ IgA+ B Cells is the Basis for IgA Deficiency: The Molecular Mechanism for Correction In Vitro by IL-10 and CD40L

2006 ◽  
Vol 26 (2) ◽  
pp. 113-125 ◽  
Author(s):  
Zaheed Husain ◽  
Nichol Holodick ◽  
Caitlin Day ◽  
Irma Szymanski ◽  
Chester A. Alper
Keyword(s):  
B Cells ◽  
Molecular Mechanism ◽  
Iga Deficiency

scholarly journals Apoptosis induced by the antigen receptor and Fas in a variant of the immature B cell line WEHI-231 and in splenic immature B cells

2001 ◽  
Vol 13 (4) ◽  
pp. 581-592 ◽  
Author(s):  
Maoxin Tim Tian ◽  
Chih-Hao Gilbert Chou ◽  
Anthony L. DeFranco
Keyword(s):  
B Cells ◽  
B Cell ◽  
Cell Line ◽  
Antigen Receptor ◽  
Wehi 231 ◽  
Immature B Cells

scholarly journals Germinal center reutilization by newly activated B cells

2009 ◽  
Vol 206 (13) ◽  
pp. 2907-2914 ◽  
Author(s):  
Tanja A. Schwickert ◽  
Boris Alabyev ◽  
Tim Manser ◽  
Michel C. Nussenzweig
Keyword(s):  
B Cells ◽  
Immune Responses ◽  
Somatic Hypermutation ◽  
Affinity Maturation ◽  
Anatomical Structures ◽  
Class Switch ◽  
Cell Clones ◽  
T Cell Help ◽  
Activated B Cells

Germinal centers (GCs) are specialized structures in which B lymphocytes undergo clonal expansion, class switch recombination, somatic hypermutation, and affinity maturation. Although these structures were previously thought to contain a limited number of isolated B cell clones, recent in vivo imaging studies revealed that they are in fact dynamic and appear to be open to their environment. We demonstrate that B cells can colonize heterologous GCs. Invasion of primary GCs after subsequent immunization is most efficient when T cell help is shared by the two immune responses; however, it also occurs when the immune responses are entirely unrelated. We conclude that GCs are dynamic anatomical structures that can be reutilized by newly activated B cells during immune responses.

scholarly journals Somatic diversification in the absence of antigen-driven responses is the hallmark of the IgM+IgD+CD27+ B cell repertoire in infants

2008 ◽  
Vol 205 (6) ◽  
pp. 1331-1342 ◽  
Author(s):  
Sandra Weller ◽  
Maria Mamani-Matsuda ◽  
Capucine Picard ◽  
Corinne Cordier ◽  
Damiana Lecoeuche ◽  
...  
Keyword(s):  
T Cell ◽  
B Cells ◽  
Immune Responses ◽  
Germinal Center ◽  
Early Stage ◽  
Cell Repertoire ◽  
Very Young Children ◽  
B Cell Repertoire ◽  
Somatic Diversification ◽  
The Many

T cell–dependent immune responses develop soon after birth, whereas it takes 2 yr for humans to develop T cell–independent responses. We used this dissociation to analyze the repertoire diversification of IgM+IgD+CD27+ B cells (also known as “IgM memory” B cells), comparing these cells with switched B cells in children <2 yr of age, with the aim of determining whether these two subsets are developmentally related. We show that the repertoire of IgM+IgD+CD27+ B cells in the spleen and blood displays no sign of antigen-driven activation and expansion on H-CDR3 spectratyping, despite the many antigenic challenges provided by childhood vaccinations. This repertoire differed markedly from those of switched B cells and splenic germinal center B cells, even at the early stage of differentiation associated with μ heavy chain expression. These data provide evidence for the developmental diversification of IgM+IgD+CD27+ B cells, at least in very young children, outside of T cell–dependent and –independent immune responses.

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