Faculty Opinions recommendation of CD24(hi)CD27(+) B cells from patients with allergic asthma have impaired regulatory activity in response to lipopolysaccharide.

Author(s):  
Gail Gauvreau ◽  
John Paul Oliveria
2014 ◽  
Vol 44 (4) ◽  
pp. 517-528 ◽  
Author(s):  
L. E. P. M. van der Vlugt ◽  
E. Mlejnek ◽  
A. Ozir-Fazalalikhan ◽  
M. Janssen Bonas ◽  
T. R. Dijksman ◽  
...  

2021 ◽  
Author(s):  
SABELO HADEBE ◽  
Anca Flavia Savulescu ◽  
Jermaine Khumalo ◽  
Katelyn Jones ◽  
Sandisiwe Mangali ◽  
...  

Abstract Allergic asthma is a disease driven by T helper 2 (Th2) cells, eosinophilia, airway hyperresponsiveness (AHR) and IgE-secreting B cells. Asthma is largely controlled by corticosteroids and β2 adregenic receptor agonists that target and relax airway smooth muscle (ASM). Immunoglobulin M (IgM) isotype secreted by naïve B cells is important for class switching but may have other undefined functions. We investigated the role of IgM in a house dust mite (HDM)-induced Th2 allergic asthma model by sensitising wild type (WT) and IgM-deficient (IgM-/-) mice with HDM. We validated our findings using CRISPR and single cell force cytometry in human ASM. We found IgM to be essential in AHR but not Th2 airway inflammation or eosinophilia. RNA sequencing of lung tissue suggested that IgM regulated AHR through modulating brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1 (Baiap2l1) and erythroid differentiation regulator 1 (Erdr1). Deletion of BAIAP2L1 and ERDR1 reduced human ASM contraction when stimulated with TNF-α. These are unprecedented findings and have implications in future treatment of asthma beyond current therapies.


1999 ◽  
Vol 67 (9) ◽  
pp. S609
Author(s):  
M. Carreno ◽  
V. Esquenazi ◽  
J. Mathew ◽  
R. Garcia-Morales ◽  
C. Gomez ◽  
...  

2019 ◽  
Vol 32 (3) ◽  
pp. 155-162 ◽  
Author(s):  
Yoshihiro Baba ◽  
Yuichi Saito ◽  
Yasuaki Kotetsu

Abstract B cells represent a key cellular component of humoral immunity. Besides antigen presentation and antibody production, B cells also play a role in immune regulation and induction of tolerance through several mechanisms. Our understanding of B-lineage cells with regulatory ability has been revolutionized by the delineation of heterogeneous subsets of these cells. Specific environmental signals may further determine the polarization and function of B-lineage regulatory cells. With the availability of new genetic, molecular and pharmacological tools, considerable advances have been made toward our understanding of the surface phenotype, developmental processes and functions of these cells. These exciting discoveries, some of which are still controversial, also raise many new questions, which makes the inhibitory function of B cells a rapidly growing field in immunopathology. Here we review highlights of the regulatory activity of B cells and the recent advances in the function and phenotype of these B-cell subsets in healthy and diseased states.


Blood ◽  
2013 ◽  
Vol 122 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Zenichiro Saze ◽  
Patrick J. Schuler ◽  
Chang-Sook Hong ◽  
Dongmei Cheng ◽  
Edwin K. Jackson ◽  
...  

Key PointsProducts of ATP hydrolysis, 5′AMP, and adenosine orchestrate the dual regulatory activity of B cells. B cells emerge as a key regulatory component of T cell–B cell interactions, which are under environmental control.


2017 ◽  
Vol 37 (4) ◽  
Author(s):  
Liming Chen ◽  
Jianfeng Xu ◽  
Xiaoxia Chu ◽  
Chenghua Ju

Thrombospondin 1 (TSP1)-producing B cells are an important immune regulatory cell fraction in the body, which are compromised in a number of immune diseases. miRs are involved in the immune regulation. The present study aims to elucidate the mechanism by which miR-98 interferes with the expression of TSP1 in B cells of the peripheral blood system. In the present study, peripheral blood samples were collected from patients with allergic asthma. The B cells were isolated from the blood samples to be analyzed for the expression of miR-98 and TSP1. The results showed that the levels of miR-98 were higher, the levels of TSP1 were lower, in B cells isolated from the peripheral blood in patients with asthma. A negative correlation was identified between the data of miR-98 and TSP1 in B cells. Exposure to T helper (Th) 2 (Th2) cytokine, interleukin (IL)-13, increased the expression of miR-98 and suppressed the expression of TSP1 in peripheral B cells, which was abolished by knocking down the miR-98 gene. In conclusion, miR-98 can suppress the expression of TSP1 in the peripheral B cells of patients with allergic asthma.


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