scholarly journals Activated Antigen-Specific CD8+T Cells Persist in the Lungs Following Recovery from Respiratory Virus Infections

2001 ◽  
Vol 166 (3) ◽  
pp. 1813-1822 ◽  
Author(s):  
Robert J. Hogan ◽  
Edward J. Usherwood ◽  
Weimin Zhong ◽  
Alan D. Roberts ◽  
Richard W. Dutton ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Respiratory Virus ◽  
Virus Infections ◽  
Respiratory Virus Infections

scholarly journals The route of priming influences the ability of respiratory virus–specific memory CD8+ T cells to be activated by residual antigen

2010 ◽  
Vol 207 (6) ◽  
pp. 1153-1160 ◽  
Author(s):  
Shiki Takamura ◽  
Alan D. Roberts ◽  
Dawn M. Jelley-Gibbs ◽  
Susan T. Wittmer ◽  
Jacob E. Kohlmeier ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
Respiratory Virus ◽  
Virus Infections ◽  
Memory Cd8 T Cells ◽  
Virus Clearance ◽  
Specific Memory ◽  
Respiratory Virus Infections ◽  
Lung Airways

After respiratory virus infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and parainfluenza virus infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. virus infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways.

scholarly journals Nonspecific Recruitment of Memory CD8+T Cells to the Lung Airways During Respiratory Virus Infections

2003 ◽  
Vol 170 (3) ◽  
pp. 1423-1429 ◽  
Author(s):  
Kenneth H. Ely ◽  
Linda S. Cauley ◽  
Alan D. Roberts ◽  
Jean W. Brennan ◽  
Tres Cookenham ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Respiratory Virus ◽  
Virus Infections ◽  
Memory Cd8 T Cells ◽  
Respiratory Virus Infections ◽  
Lung Airways

scholarly journals Interstitial-resident memory CD8+ T cells sustain frontline epithelial memory in the lung

2019 ◽  
Vol 216 (12) ◽  
pp. 2736-2747 ◽  
Author(s):  
Shiki Takamura ◽  
Shigeki Kato ◽  
Chihiro Motozono ◽  
Takeshi Shimaoka ◽  
Satoshi Ueha ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Population ◽  
Cd8 T Cells ◽  
Respiratory Virus ◽  
Effector Memory ◽  
Homeostatic Proliferation ◽  
Virus Infections ◽  
Memory Cd8 T Cells ◽  
Respiratory Virus Infections ◽  
Lung Airways

Populations of CD8+ lung-resident memory T (TRM) cells persist in the interstitium and epithelium (airways) following recovery from respiratory virus infections. While it is clear that CD8+ TRM cells in the airways are dynamically maintained via the continuous recruitment of new cells, there is a vigorous debate about whether tissue-circulating effector memory T (TEM) cells are the source of these newly recruited cells. Here we definitively demonstrate that CD8+ TRM cells in the lung airways are not derived from TEM cells in the circulation, but are seeded continuously by TRM cells from the lung interstitium. This process is driven by CXCR6 that is expressed uniquely on TRM cells but not TEM cells. We further demonstrate that the lung interstitium CD8+ TRM cell population is also maintained independently of TEM cells via a homeostatic proliferation mechanism. Taken together, these data show that lung memory CD8+ TRM cells in the lung interstitium and airways are compartmentally separated from TEM cells and clarify the mechanisms underlying their maintenance.

scholarly journals Reinfection with SARS-CoV-2: Implications for Vaccines

2020 ◽  
Author(s):  
Jeffrey I Cohen ◽  
Peter D Burbelo
Keyword(s):  
T Cells ◽  
Protective Immunity ◽  
Respiratory Virus ◽  
Virus Infections ◽  
Serum Antibodies ◽  
Protective Measures ◽  
Respiratory Virus Infections

Abstract Infection with SARS-CoV-2 has become pandemic and the duration of protective immunity to the virus is unknown. Cases of persons reinfected with the virus are being reported with increasing frequency. At present it is unclear how common reinfection with SARS-CoV-2 is and how long serum antibodies and virus-specific T cells persist after infection. For many other respiratory virus infections, including influenza and the seasonal coronaviruses that cause colds, serum antibodies persist for only months to a few years and reinfections are very common. Here we review what is known about the duration of immunity and reinfection with coronaviruses, including SARS-CoV-2, and well as the duration of immunity to other viruses and virus vaccines. These findings have implications for the need of continued protective measures and for vaccines for persons previously infected with SARS-CoV-2.

scholarly journals Protection from Respiratory Virus Infections Can Be Mediated by Antigen-Specific Cd4+ T Cells That Persist in the Lungs

2001 ◽  
Vol 193 (8) ◽  
pp. 981-986 ◽  
Author(s):  
Robert J. Hogan ◽  
Weimin Zhong ◽  
Edward J. Usherwood ◽  
Tres Cookenham ◽  
Alan D. Roberts ◽  
...  
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Cellular Immunity ◽  
Cd4 T Cells ◽  
Respiratory Virus ◽  
Critical Role ◽  
Lymphoid Tissues ◽  
Virus Infections ◽  
Respiratory Virus Infections ◽  
Memory Cd4 T Cells

Although CD4+ T cells have been shown to mediate protective cellular immunity against respiratory virus infections, the underlying mechanisms are poorly understood. For example, although phenotypically distinct populations of memory CD4+ T cells have been identified in different secondary lymphoid tissues, it is not known which subpopulations mediate protective cellular immunity. In this report, we demonstrate that virus-specific CD4+ T cells persist in the lung tissues and airways for several months after Sendai virus infection of C57BL/6 mice. A large proportion of these cells possess a highly activated phenotype (CD44hi, CD62Llo, CD43hi, and CD25hi) and express immediate effector function as indicated by the production of interferon γ after a 5-h restimulation in vitro. Furthermore, intratracheal adoptive transfer of lung memory cells into β2m-deficient mice demonstrated that lung-resident virus-specific CD4+ T cells mediated a substantial degree of protection against secondary virus infection. Taken together, these data demonstrate that activated memory CD4+ T cells persisting at mucosal sites play a critical role in mediating protective cellular immunity.

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