Defective B-cell Response to Toll-like Receptor-9 Ligands in Common Variable Immunodeficiency

2010 ◽  
Vol 10 (5) ◽  
pp. 303-305
Author(s):  
Julie Y. Patel ◽  
Sapandeep K. Singh ◽  
David P. Huston
Keyword(s):  
B Cell ◽  
Common Variable Immunodeficiency ◽  
Cell Response ◽  
Toll Like Receptor ◽  
Common Variable ◽  
B Cell Response

scholarly journals Defective Toll-Like Receptors Driven B Cell Response in Hyper IgE Syndrome Patients With STAT3 Mutations

2021 ◽  
Vol 9 ◽  
Author(s):  
Ruolan Gong ◽  
Jing Wu ◽  
Yingying Jin ◽  
Tongxin Chen
Keyword(s):  
B Cell ◽  
Cell Response ◽  
Gene Mutations ◽  
Toll Like Receptor ◽  
Cell Responses ◽  
Hyper Ige Syndrome ◽  
Class Switch ◽  
Cell Class ◽  
Stat3 Mutations ◽  
B Cell Response

Autosomal dominant hyper-IgE syndrome (AD-HIES) is a rare inherited primary immunodeficient disease (PIDs), which is caused by STAT3 gene mutations. Previous studies indicated a defective Toll-like receptor (TLR) 9-induced B cell response in AD-HIES patients, including proliferation, and IgG production. However, the other TLRs-mediated B cell responses in AD-HIES patients were not fully elucidated. In this study, we systematically studied the B cell response to TLRs signaling pathways in AD-HIES patients, including proliferation, activation, apoptosis, cytokine, and immunoglobulin production. Our results showed that the TLRs-induced B cell proliferation and activation was significantly impaired in AD-HIES patients. Besides, AD-HIES patients had defects in TLRs-induced B cell class switch, as well as IgG/IgM secretion and IL-10 production in B cells. Taken together, we first systematically reported the deficiency of TLRs driven B cell response in AD-HIES patients, which help to have a better understanding of the pathology of AD-HIES.

scholarly journals CD72 negatively regulates B lymphocyte responses to the lupus-related endogenous toll-like receptor 7 ligand Sm/RNP

2016 ◽  
Vol 213 (12) ◽  
pp. 2691-2706 ◽  
Author(s):  
Chizuru Akatsu ◽  
Kenro Shinagawa ◽  
Nobutaka Numoto ◽  
Zhihong Liu ◽  
Ayse Konuskan Ucar ◽  
...  
Keyword(s):  
B Cell ◽  
Lupus Erythematosus ◽  
Cell Response ◽  
B Lymphocyte ◽  
Crystallographic Analysis ◽  
Autoimmune Response ◽  
Toll Like Receptor ◽  
Lymphocyte Responses ◽  
Tlr7 Ligand ◽  
B Cell Response

Toll-like receptor 7 (TLR7) plays an essential role in development of systemic lupus erythematosus by co-stimulating B cells reactive to the endogenous TLR7 ligand Sm/ribonucleoprotein (RNP), a crucial lupus self-antigen. However, how the TLR7-mediated autoimmune response is regulated is not yet known. In this study, we demonstrate that CD72, an inhibitory B cell co-receptor known to prevent development of lupus, recognizes Sm/RNP at the extracellular C-type lectin-like domain (CTLD) and specifically inhibits B cell response to Sm/RNP. Moreover, the CTLD of CD72c, a lupus-susceptible allele, binds to Sm/RNP less strongly than that of lupus-resistant CD72a. Reduced binding of CD72c is supported by x-ray crystallographic analysis that reveals a considerable alteration in charge at the putative ligand-binding site. Thus, CD72 appears to specifically inhibit B cell response to the endogenous TLR7 ligand Sm/RNP through CTLD-mediated recognition of Sm/RNP, thereby preventing production of anti-Sm/RNP antibody crucial for development of lupus.

225 The allergen specific B-cell response during immunotherapy

1991 ◽  
Vol 87 (1) ◽  
pp. 195
Author(s):  
S SPARHOLT ◽  
H LOWENSTEIN ◽  
C SCHOU
Keyword(s):  
B Cell ◽  
Cell Response ◽  
B Cell Response

scholarly journals B cell activation by cytomegalovirus.

1983 ◽  
Vol 158 (6) ◽  
pp. 2171-2176 ◽  
Author(s):  
L M Hutt-Fletcher ◽  
N Balachandran ◽  
M H Elkins
Keyword(s):  
T Cell ◽  
B Cell ◽  
Virus Replication ◽  
Human Cytomegalovirus ◽  
Cell Response ◽  
Cell Activation ◽  
B Cell Activation ◽  
T Cell Help ◽  
Cell Activator ◽  
B Cell Response

Human cytomegalovirus is shown to be a nonspecific polyclonal B cell activator. The B cell response is independent of virus replication and requires little, if any, T cell help.

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