scholarly journals Effects of Developmental Activation of the AhR on CD4+T-Cell Responses to Influenza Virus Infection in Adult Mice

2014 ◽  
Vol 122 (11) ◽  
pp. 1201-1208 ◽  
Author(s):  
Lisbeth A. Boule ◽  
Bethany Winans ◽  
B. Paige Lawrence
2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
John Ross Teijaro ◽  
Modesta Ndejembi ◽  
Smita Chandran ◽  
Donna Farber

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Masaaki Miyazawa

Abstract Factors determining the progression of frequently mild or asymptomatic severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection into life-threatening pneumonia remain poorly understood. Viral and host factors involved in the development of diffuse alveolar damage have been extensively studied in influenza virus infection. Influenza is a self-limited upper respiratory tract infection that causes acute and severe systemic symptoms and its spread to the lungs is limited by CD4+ T-cell responses. A vicious cycle of CCL2- and CXCL2-mediated inflammatory monocyte and neutrophil infiltration and activation and resultant massive production of effector molecules including tumor necrosis factor (TNF)-α, nitric oxide, and TNF-related apoptosis-inducing ligand are involved in the pathogenesis of progressive tissue injury. SARS-CoV-2 directly infects alveolar epithelial cells and macrophages and induces foci of pulmonary lesions even in asymptomatic individuals. Mechanisms of tissue injury in SARS-CoV-2-induced pneumonia share some aspects with influenza virus infection, but IL-1β seems to play more important roles along with CCL2 and impaired type I interferon signaling might be associated with delayed virus clearance and disease severity. Further, data indicate that preexisting memory CD8+ T cells may play important roles in limiting viral spread in the lungs and prevent progression from mild to severe or critical pneumonia. However, it is also possible that T-cell responses are involved in alveolar interstitial inflammation and perhaps endothelial cell injury, the latter of which is characteristic of SARS-CoV-2-induced pathology.


2016 ◽  
Vol 12 (7) ◽  
pp. e1005754 ◽  
Author(s):  
Matheswaran Kandasamy ◽  
Amol Suryawanshi ◽  
Smanla Tundup ◽  
Jasmine T. Perez ◽  
Mirco Schmolke ◽  
...  

2020 ◽  
Author(s):  
Emily L Goldberg ◽  
Akiko Iwasaki ◽  
Vishwa Deep Dixit

We are glad for the broad interest and readership our recent publication “Ketogenic diet activates protective γδ T cell responses against influenza virus infection” has received. The goal of our study was to understand how the immune system might be involved in mediating the surprising protection against lethal influenza A virus infection we observed when we fed mice a ketogenic diet (KD) for one week. What made our findings particularly intriguing is that robust protective changes were occurring in the lungs, the site of influenza infection and, importantly, not a tissue traditionally considered in manipulations of systemic metabolism, and that these protective changes were γδ T cell-dependent. Amidst this enthusiasm, Bass et al. have raised concern about the control diets used in our experiments, specifically with regards to the protein, fiber, and micronutrient content. We welcome critical feedback and appreciate the opportunity to respond to these criticisms.


2004 ◽  
Vol 17 (2) ◽  
pp. 197-209 ◽  
Author(s):  
Susan L. Swain ◽  
Richard W. Dutton ◽  
David L. Woodland

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