scholarly journals Regulatory CD8+T Cells Associated with Erosion of Immune Surveillance in Persistent Virus Infection Suppress In Vitro and Have a Reversible Proliferative Defect

2013 ◽  
Vol 191 (1) ◽  
pp. 312-322 ◽  
Author(s):  
Zhuting Hu ◽  
Weijun Zhang ◽  
Edward J. Usherwood
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
Immune Surveillance ◽  
Persistent Virus Infection ◽  
Persistent Virus

scholarly journals Overcoming CD4 Th1 Cell Fate Restrictions to Sustain Antiviral CD8 T Cells and Control Persistent Virus Infection

Cell Reports ◽  
2016 ◽  
Vol 16 (12) ◽  
pp. 3286-3296 ◽  
Author(s):  
Laura M. Snell ◽  
Ivan Osokine ◽  
Douglas H. Yamada ◽  
Justin Rafael De la Fuente ◽  
Heidi J. Elsaesser ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Cell Fate ◽  
Cd8 T Cells ◽  
Th1 Cell ◽  
Persistent Virus Infection ◽  
Persistent Virus ◽  
And Control

scholarly journals Virus-specific CD8+ cells can switch to interleukin 5 production and induce airway eosinophilia.

1995 ◽  
Vol 181 (3) ◽  
pp. 1229-1233 ◽  
Author(s):  
A J Coyle ◽  
F Erard ◽  
C Bertrand ◽  
S Walti ◽  
H Pircher ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Virus Infection ◽  
Immune Responses ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Eosinophil Infiltration ◽  
Virus Infections ◽  
Cd8 Cells

Virus infections of the lung are thought to predispose individuals to asthma, a disease characterized by eosinophil infiltration of the airways. CD8+ T cells are an important part of the host response to virus infection, however, they have no reported role in eosinophil recruitment. We developed a mouse model of virus peptide-stimulated CD8+ T cell immune responses in the lung. We found that bystander CD4+ T helper cell type 2 immune responses to ovalbumin switched the virus peptide-specific CD8+ T cells in the lung to interleukin (IL) 5 production. Furthermore, when such IL-5-producing CD8 T cells were challenged via the airways with virus peptide, a significant eosinophil infiltration was induced. In vitro studies indicated that IL-4 could switch the virus-specific CD8+ T cells to IL-5 production. These results could explain the link between virus infection and acute exacerbation of asthma and, perhaps more importantly, they indicate an IL-4-dependent mechanism that would impair CD8+ T cell responses and delay viral clearance from the host.

scholarly journals TRMintegrins CD103 and CD49a differentially support adherence and motility after resolution of influenza virus infection

2020 ◽  
Vol 117 (22) ◽  
pp. 12306-12314 ◽  
Author(s):  
Emma C. Reilly ◽  
Kris Lambert Emo ◽  
Patrick M. Buckley ◽  
Nicholas S. Reilly ◽  
Ian Smith ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
Expression Patterns ◽  
Influenza Virus Infection ◽  
Immune Memory ◽  
Peripheral Tissues ◽  
Established Role

Tissue-resident memory CD8 T (TRM) cells are a unique immune memory subset that develops and remains in peripheral tissues at the site of infection, providing future host resistance upon reexposure to that pathogen. In the pulmonary system, TRMare identified through S1P antagonist CD69 and expression of integrins CD103/β7 and CD49a/CD29(β1). Contrary to the established role of CD69 on CD8 T cells, the functions of CD103 and CD49a on this population are not well defined. This study examines the expression patterns and functions of CD103 and CD49a with a specific focus on their impact on T cell motility during influenza virus infection. We show that the TRMcell surface phenotype develops by 2 wk postinfection, with the majority of the population expressing CD49a and a subset that is also positive for CD103. Despite a previously established role in retaining TRMin peripheral tissues, CD49a facilitates locomotion of virus-specific CD8 T cells, both in vitro and in vivo. These results demonstrate that CD49a may contribute to local surveillance mechanisms of the TRMpopulation.

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