Ex Vivo Characterization of the Epitope-Specific T Cell Response to Alternaria

2012 ◽  
Vol 129 (2) ◽  
pp. AB197
Author(s):  
J.H. DeLong ◽  
E. Wambre ◽  
R. LaFond ◽  
N. Torres-Chinn ◽  
E.A. James ◽  
...  
Keyword(s):  
T Cell ◽  
Ex Vivo ◽  
2011 ◽  
Vol 127 (2) ◽  
pp. AB257-AB257
Author(s):  
J.H. DeLong ◽  
K. Hetherington ◽  
E. Wambre ◽  
D. Robinson ◽  
W.W. Kwok

2013 ◽  
Vol 68 (6) ◽  
pp. 357-368 ◽  
Author(s):  
Marie Baeck ◽  
Angèle Soria ◽  
Liliane Marot ◽  
Ivan Theate ◽  
Emilie Hendrickx ◽  
...  

1982 ◽  
Vol 156 (3) ◽  
pp. 822-833 ◽  
Author(s):  
C N Baxevanis ◽  
N Ishii ◽  
Z A Nagy ◽  
J Klein

We characterized the cell types involved in the H-2-controlled suppression of T cell response to lactate dehydrogenase B (LDHB). The suppressor effector (Tse) was found to be an Lyt-1+2+, J+ cell that recognizes antigen together with Ek molecules of antigen-presenting cells (APC). To become functional, the Tse cell requires a second signal from a nonspecific, Lyt-1+2-, J+ suppressor-inducer (Tsi) cell. The Tsi-Tse interaction is not subject to any genetic restriction. The target cell of suppression is an Lyt-1+2-, J- (most likely T helper [Th]) cell that recognizes LDHB in the context of A molecules on APC. The suppression is manifested in inhibition of the antigen-specific, A-restricted proliferation of Th cells. The interaction between Tse and Th is restricted by the A region of the H-2 complex. Because this restriction is determined by the receptor of Th cells, the mechanism of Th-Tse interaction most likely involves a concomitant recognition of LDHB and A region-controlled molecules by Th cells on the surface of Tse cells.


2003 ◽  
Vol 77 (9) ◽  
pp. 5226-5240 ◽  
Author(s):  
Rebecca Elkington ◽  
Susan Walker ◽  
Tania Crough ◽  
Moira Menzies ◽  
Judy Tellam ◽  
...  

ABSTRACT Human cytomegalovirus (HCMV) can establish both nonproductive (latent) and productive (lytic) infections. Many of the proteins expressed during these phases of infection could be expected to be targets of the immune response; however, much of our understanding of the CD8+-T-cell response to HCMV is mainly based on the pp65 antigen. Very little is known about T-cell control over other antigens expressed during the different stages of virus infection; this imbalance in our understanding undermines the importance of these antigens in several aspects of HCMV disease pathogenesis. In the present study, an efficient and rapid strategy based on predictive bioinformatics and ex vivo functional T-cell assays was adopted to profile CD8+-T-cell responses to a large panel of HCMV antigens expressed during different phases of replication. These studies revealed that CD8+-T-cell responses to HCMV often contained multiple antigen-specific reactivities, which were not just constrained to the previously identified pp65 or IE-1 antigens. Unexpectedly, a number of viral proteins including structural, early/late antigens and HCMV-encoded immunomodulators (pp28, pp50, gH, gB, US2, US3, US6, and UL18) were also identified as potential targets for HCMV-specific CD8+-T-cell immunity. Based on this extensive analysis, numerous novel HCMV peptide epitopes and their HLA-restricting determinants recognized by these T cells have been defined. These observations contrast with previous findings that viral interference with the antigen-processing pathway during lytic infection would render immediate-early and early/late proteins less immunogenic. This work strongly suggests that successful HCMV-specific immune control in healthy virus carriers is dependent on a strong T-cell response towards a broad repertoire of antigens.


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