scholarly journals Co-Ordination of Mucosal B Cell and CD8 T Cell Memory by Tissue-Resident CD4 Helper T Cells

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2355
Author(s):  
Young Min Son ◽  
Jie Sun

Adaptive cellular immunity plays a major role in clearing microbial invasion of mucosal tissues in mammals. Following the clearance of primary pathogens, memory lymphocytes are established both systemically and locally at pathogen entry sites. Recently, resident memory CD8 T and B cells (TRM and BRM respectively), which are parked mainly in non-lymphoid mucosal tissues, were characterized and demonstrated to be essential for protection against secondary microbial invasion. Here we reviewed the current understanding of the cellular and molecular cues regulating CD8 TRM and BRM development, maintenance and function. We focused particularly on elucidating the role of a novel tissue-resident helper T (TRH) cell population in assisting TRM and BRM responses in the respiratory mucosa following viral infection. Finally, we argue that the promotion of TRH responses by future mucosal vaccines would be key to the development of successful universal influenza or coronavirus vaccines, providing long-lasting immunity against a broad spectrum of viral strains.

2017 ◽  
Vol 114 (48) ◽  
pp. 12797-12802 ◽  
Author(s):  
A. Ripamonti ◽  
E. Provasi ◽  
M. Lorenzo ◽  
M. De Simone ◽  
V. Ranzani ◽  
...  

Follicular helper T cells (TFHs) are a key component of adaptive immune responses as they help antibody production by B cells. Differentiation and function of TFH cells are controlled by the master gene BCL6, but it is largely unclear how this transcription repressor specifies the TFH program. Here we asked whether BCL6 controlled helper function through down-regulation of specific microRNAs (miRNAs). We first assessed miRNA expression in TFH cells and defined a TFH-specific miRNA signature. We report that hsa–miR-31–5p (miR-31) is down-regulated in TFH; we showed that BCL6 suppresses miR-31 expression by binding to its promoter; and we demonstrated that miR-31 inhibits the expression of molecules that control T-helper function, such as CD40L and SAP. These findings identify a BCL6-initiated inhibitory circuit that stabilizes the follicular helper T cell program at least in part through the control of miRNA transcription. Although BCL6 controls TFH activity in human and mouse, the role of miR-31 is restricted to human TFH cell differentiation, reflecting a species specificity of the miR-31 action. Our findings highlight miR-31 as a possible target to modulate human T cell dependent antibody responses in the settings of infection, vaccination, or immune dysregulation.


2012 ◽  
Vol 190 (3) ◽  
pp. 1066-1075 ◽  
Author(s):  
Fanny Tzelepis ◽  
Julie Joseph ◽  
Elias K. Haddad ◽  
Susanne MacLean ◽  
Renu Dudani ◽  
...  

2005 ◽  
Vol 5 (2) ◽  
pp. 101-111 ◽  
Author(s):  
Rustom Antia ◽  
Vitaly V. Ganusov ◽  
Rafi Ahmed

2003 ◽  
Vol 171 (10) ◽  
pp. 5454-5460 ◽  
Author(s):  
Yvan Chapdelaine ◽  
Dean K. Smith ◽  
Joao A. Pedras-Vasconcelos ◽  
Lakshmi Krishnan ◽  
Subash Sad

2012 ◽  
Vol 55 (1-3) ◽  
pp. 135-145 ◽  
Author(s):  
Lindsay E. Edwards ◽  
Catherine Haluszczak ◽  
Ross M. Kedl

Cells ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 51
Author(s):  
William P. Lafuse ◽  
Daniel J. Wozniak ◽  
Murugesan V. S. Rajaram

The immune system plays a pivotal role in the initiation, development and resolution of inflammation following insult or damage to organs. The heart is a vital organ which supplies nutrients and oxygen to all parts of the body. Heart failure (HF) has been conventionally described as a disease associated with cardiac tissue damage caused by systemic inflammation, arrhythmia and conduction defects. Cardiac inflammation and subsequent tissue damage is orchestrated by the infiltration and activation of various immune cells including neutrophils, monocytes, macrophages, eosinophils, mast cells, natural killer cells, and T and B cells into the myocardium. After tissue injury, monocytes and tissue-resident macrophages undergo marked phenotypic and functional changes, and function as key regulators of tissue repair, regeneration and fibrosis. Disturbance in resident macrophage functions such as uncontrolled production of inflammatory cytokines, growth factors and inefficient generation of an anti-inflammatory response or unsuccessful communication between macrophages and epithelial and endothelial cells and fibroblasts can lead to aberrant repair, persistent injury, and HF. Therefore, in this review, we discuss the role of cardiac macrophages on cardiac inflammation, tissue repair, regeneration and fibrosis.


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