scholarly journals The Chemokine Receptor CXCR3 Promotes CD8+ T Cell Accumulation in Uninfected Salivary Glands but Is Not Necessary after Murine Cytomegalovirus Infection

2017 ◽  
Vol 200 (3) ◽  
pp. 1133-1145 ◽  
Author(s):  
Sofia Caldeira-Dantas ◽  
Thomas Furmanak ◽  
Corinne Smith ◽  
Michael Quinn ◽  
Leyla Y. Teos ◽  
...  
2006 ◽  
Vol 177 (1) ◽  
pp. 450-458 ◽  
Author(s):  
Michael W. Munks ◽  
Kathy S. Cho ◽  
Amelia K. Pinto ◽  
Sophie Sierro ◽  
Paul Klenerman ◽  
...  

2011 ◽  
Vol 7 (10) ◽  
pp. e1002313 ◽  
Author(s):  
Nicole Torti ◽  
Senta M. Walton ◽  
Thomas Brocker ◽  
Thomas Rülicke ◽  
Annette Oxenius

2009 ◽  
Vol 183 (6) ◽  
pp. 3932-3941 ◽  
Author(s):  
Christopher M. Snyder ◽  
Andrea Loewendorf ◽  
Elizabeth L. Bonnett ◽  
Michael Croft ◽  
Chris A. Benedict ◽  
...  

Pathogens ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 956
Author(s):  
Kirsten Freitag ◽  
Sara Hamdan ◽  
Matthias J. Reddehase ◽  
Rafaela Holtappels

CD8+ T-cell responses to pathogens are directed against infected cells that present pathogen-encoded peptides on MHC class-I molecules. Although natural responses are polyclonal, the spectrum of peptides that qualify for epitopes is remarkably small even for pathogens with high coding capacity. Among those few that are successful at all, a hierarchy exists in the magnitude of the response that they elicit in terms of numbers of CD8+ T cells generated. This led to a classification into immunodominant and non-immunodominant or subordinate epitopes, IDEs and non-IDEs, respectively. IDEs are favored in the design of vaccines and are chosen for CD8+ T-cell immunotherapy. Using murine cytomegalovirus as a model, we provide evidence to conclude that epitope hierarchy reflects competition on the level of antigen recognition. Notably, high-avidity cells specific for non-IDEs were found to expand only when IDEs were deleted. This may be a host’s back-up strategy to avoid viral immune escape through antigenic drift caused by IDE mutations. Importantly, our results are relevant for the design of vaccines based on cytomegaloviruses as vectors to generate high-avidity CD8+ T-cell memory specific for unrelated pathogens or tumors. We propose the deletion of vector-encoded IDEs to avoid the suppression of epitopes of the vaccine target.


Blood ◽  
2004 ◽  
Vol 104 (12) ◽  
pp. 3463-3471 ◽  
Author(s):  
Christoph Hess ◽  
Terry K. Means ◽  
Patrick Autissier ◽  
Tonia Woodberry ◽  
Marcus Altfeld ◽  
...  

CD8 T cells play a key role in host defense against intracellular pathogens. Efficient migration of these cells into sites of infection is therefore intimately linked to their effector function. The molecular mechanisms that control CD8 T-cell trafficking into sites of infection and inflammation are not well understood, but the chemokine/chemokine receptor system is thought to orchestrate this process. Here we systematically examined the chemokine receptor profile expressed on human CD8 T cells. Surprisingly, we found that CXC chemokine receptor 1 (CXCR1), the predominant neutrophil chemokine receptor, defined a novel interleukin-8/CXC ligand 8 (IL-8/CXCL8)–responsive CD8 T-cell subset that was enriched in perforin, granzyme B, and interferon-γ (IFNγ), and had high cytotoxic potential. CXCR1 expression was down-regulated by antigen stimulation both in vitro and in vivo, suggesting antigen-dependent shaping of the migratory characteristics of CD8 T cells. On virus-specific CD8 T cells from persons with a history of Epstein-Barr virus (EBV) and influenza infection, CXCR1 expression was restricted to terminally differentiated effector memory cells. In HIV-1 infection, CXCR1-expressing HIV-1–specific CD8 T cells were present only in persons who were able to control HIV-1 replication during structured treatment interruptions. Thus, CXCR1 identifies a subset of CD8 T cells poised for immediate cytotoxicity and early recruitment into sites of innate immune system activation.


2014 ◽  
Vol 34 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Erlie Jiang ◽  
Xiaoyuan Dai Perrard ◽  
Donglin Yang ◽  
Ilvira M. Khan ◽  
Jerry L. Perrard ◽  
...  

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