Memory CD8+ T cells vary in differentiation phenotype in different persistent virus infections

2002 ◽  
Vol 8 (4) ◽  
pp. 379-385 ◽  
Author(s):  
Victor Appay ◽  
P. Rod Dunbar ◽  
Margaret Callan ◽  
Paul Klenerman ◽  
Geraldine M.A. Gillespie ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Virus Infections ◽  
Memory Cd8 T Cells ◽  
Persistent Virus

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 PD-1 is a regulator of virus-specific CD8+ T cell survival in HIV infection

2006 ◽  
Vol 203 (10) ◽  
pp. 2281-2292 ◽  
Author(s):  
Constantinos Petrovas ◽  
Joseph P. Casazza ◽  
Jason M. Brenchley ◽  
David A. Price ◽  
Emma Gostick ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Cd8 T Cell ◽  
Antigen Specificity ◽  
Chronic Infections ◽  
Human Virus ◽  
Memory Cd8 T Cells ◽  
Persistent Virus

Here, we report on the expression of programmed death (PD)-1 on human virus-specific CD8+ T cells and the effect of manipulating signaling through PD-1 on the survival, proliferation, and cytokine function of these cells. PD-1 expression was found to be low on naive CD8+ T cells and increased on memory CD8+ T cells according to antigen specificity. Memory CD8+ T cells specific for poorly controlled chronic persistent virus (HIV) more frequently expressed PD-1 than memory CD8+ T cells specific for well-controlled persistent virus (cytomegalovirus) or acute (vaccinia) viruses. PD-1 expression was independent of maturational markers on memory CD8+ T cells and was not directly associated with an inability to produce cytokines. Importantly, the level of PD-1 surface expression was the primary determinant of apoptosis sensitivity of virus-specific CD8+ T cells. Manipulation of PD-1 led to changes in the ability of the cells to survive and expand, which, over several days, affected the number of cells expressing cytokines. Therefore, PD-1 is a major regulator of apoptosis that can impact the frequency of antiviral T cells in chronic infections such as HIV, and could be manipulated to improve HIV-specific CD8+ T cell numbers, but possibly not all functions in vivo.

scholarly journals Qualitatively Different Memory CD8+T Cells Are Generated after Lymphocytic Choriomeningitis Virus and Influenza Virus Infections

2010 ◽  
Vol 185 (4) ◽  
pp. 2182-2190 ◽  
Author(s):  
Scott N. Mueller ◽  
William A. Langley ◽  
Guimei Li ◽  
Adolfo García-Sastre ◽  
Richard J. Webby ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Cd8 T Cells ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Virus Infections ◽  
Memory Cd8 T Cells

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 Memory CD8 + T cells in HIV infection

2000 ◽  
Vol 355 (1395) ◽  
pp. 363-367 ◽  
Author(s):  
Andrew J. McMichael ◽  
Graham Ogg ◽  
Jamie Wilson ◽  
Margaret Callan ◽  
Sophie Hambleton ◽  
...  
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Cd8 T Cells ◽  
T Helper Cells ◽  
Hla Class I ◽  
Interferon Γ ◽  
Virus Infections ◽  
T Helper ◽  
Memory Cd8 T Cells ◽  
Turn Over

Cytotoxic T lymphocytes (CTLs) play a central role in the control of persistent HIV infection in humans. The kinetics and general features of the CTL response are similar to those found during other persisting virus infections in humans. During chronic infection there are commonly between 0.1 and 1.0% of all CD8 + T cells in the blood that are specific for immunodominant virus epitopes, as measured by HLA class I peptide tetramers. These figures are greatly in excess of the numbers found by limiting dilution assays; the discrepancy may arise because in the latter assay, CTLs have to divide many times to be detected and many of the HIV–specific CD8 + T cells circulating in infected persons may be incapable of further division. Many tetramer–positive T cells make interferon–γ, β–chemokines and perforin, so are probably functional. It is not known how fast these T cells turn over, but in the absence of antigen they decay in number. Impairment of CTL replacement, because CD4 + T helper cells are depleted by HIV infection, may play a major role in the development of AIDS.

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.

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