CYTOTOXIC T CELL RECOGNITION OF ECTROMELIA VIRUS-INFECTED CELLS.

1978 ◽  
Vol 56 (1) ◽  
pp. 69-80 ◽  
Author(s):  
Robert V Blanden ◽  
Tikky Pang
Keyword(s):  
T Cell ◽  
Cytotoxic T Cell ◽  
Cell Recognition ◽  
Ectromelia Virus ◽  
T Cell Recognition ◽  
Infected Cells

scholarly journals Primary HIV-1 Strains Use Nef To Downmodulate HLA-E Surface Expression

2019 ◽  
Vol 93 (20) ◽  
Author(s):  
Thomas van Stigt Thans ◽  
Janet I. Akko ◽  
Annika Niehrs ◽  
Wilfredo F. Garcia-Beltran ◽  
Laura Richert ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Line ◽  
Nk Cell ◽  
Cytoplasmic Tail ◽  
Cytotoxic T Cell ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Infected Cells ◽  
Hiv 1

ABSTRACTHuman immunodeficiency virus type 1 (HIV-1) has evolved elaborate ways to evade immune cell recognition, including downregulation of classical HLA class I (HLA-I) from the surfaces of infected cells. Recent evidence identified HLA-E, a nonclassical HLA-I, as an important part of the antiviral immune response to HIV-1. Changes in HLA-E surface levels and peptide presentation can prompt both CD8+T-cell and natural killer (NK) cell responses to viral infections. Previous studies reported unchanged or increased HLA-E levels on HIV-1-infected cells. Here, we examined HLA-E surface levels following infection of CD4+T cells with primary HIV-1 strains and observed that a subset downregulated HLA-E. Two primary strains of HIV-1 that induced the strongest reduction in surface HLA-E expression were chosen for further testing. Expression of single Nef or Vpu proteins in a T-cell line, as well as tail swap experiments exchanging the cytoplasmic tail of HLA-A2 with that of HLA-E, demonstrated that Nef modulated HLA-E surface levels and targeted the cytoplasmic tail of HLA-E. Furthermore, infection of primary CD4+T cells with HIV-1 mutants showed that a lack of functional Nef (and Vpu to some extent) impaired HLA-E downmodulation. Taken together, the results of this study demonstrate for the first time that HIV-1 can downregulate HLA-E surface levels on infected primary CD4+T cells, potentially rendering them less vulnerable to CD8+T-cell recognition but at increased risk of NKG2A+NK cell killing.IMPORTANCEFor almost two decades, it was thought that HIV-1 selectively downregulated the highly expressed HLA-I molecules HLA-A and HLA-B from the cell surface in order to evade cytotoxic-T-cell recognition, while leaving HLA-C and HLA-E molecules unaltered. It was stipulated that HIV-1 infection thereby maintained inhibition of NK cells via inhibitory receptors that bind HLA-C and HLA-E. This concept was recently revised when a study showed that primary HIV-1 strains reduce HLA-C surface levels, whereas the cell line-adapted HIV-1 strain NL4-3 lacks this ability. Here, we demonstrate that infection with distinct primary HIV-1 strains results in significant downregulation of surface HLA-E levels. Given the increasing evidence for HLA-E as an important modulator of CD8+T-cell and NKG2A+NK cell functions, this finding has substantial implications for future immunomodulatory approaches aimed at harnessing cytotoxic cellular immunity against HIV.

scholarly journals CD8+ T-cell recognition of human cytomegalovirus latency-associated determinant pUL138

2010 ◽  
Vol 91 (8) ◽  
pp. 2040-2048 ◽  
Author(s):  
Siok-Keen Tey ◽  
Felicia Goodrum ◽  
Rajiv Khanna
Keyword(s):  
T Cells ◽  
T Cell ◽  
Human Cytomegalovirus ◽  
Cell Response ◽  
Hcmv Infection ◽  
Mononuclear Cells ◽  
T Cell Response ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Infected Cells

Recent studies have shown that long-term persistence of human cytomegalovirus (HCMV) in mononuclear cells of myeloid lineage is dependent on the UL138 open reading frame, which promotes latent infection. Although T-cell recognition of protein antigens from all stages of lytic HCMV infection is well established, it is not clear whether proteins expressed during latent HCMV infection can also be recognized. This study conducted an analysis of T-cell response towards proteins associated with HCMV latency. Ex vivo analysis of T cells from healthy virus carriers revealed a dominant CD8+ T-cell response to the latency-associated pUL138 protein, which recognized a non-canonical 13 aa epitope in association with HLA-B*3501. These pUL138-specific T cells displayed a range of memory phenotypes that were in general less differentiated than that previously described in T cells specific for HCMV lytic antigens. Antigen-presentation assays revealed that endogenous pUL138 could be presented efficiently by HCMV-infected cells. However, T-cell recognition of pUL138 was dependent on newly synthesized protein, with little presentation from stable, long-lived protein. These data demonstrate that T cells targeting latency-associated protein products exist, although HCMV may limit the presentation of latent proteins, thereby restricting T-cell recognition of latently infected cells.

Cytotoxic T Cell Recognition of the SV40 Tumor Antigen: A Note of Caution

1988 ◽  
pp. 87-95 ◽  
Author(s):  
LINDA R. GOODING ◽  
KATHRYN A. O'CONNELL ◽  
ROY GEIB ◽  
JAMES M. PIPAS
Keyword(s):  
T Cell ◽  
Tumor Antigen ◽  
Cytotoxic T Cell ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Antigen A

scholarly journals Two Salmonella OmpC Kb-Restricted Epitopes for CD8+-T-Cell Recognition

2004 ◽  
Vol 72 (5) ◽  
pp. 3059-3062 ◽  
Author(s):  
Alberto Diaz-Quiñonez ◽  
Natalia Martin-Orozco ◽  
Armando Isibasi ◽  
Vianney Ortiz-Navarrete
Keyword(s):  
T Cell ◽  
Cytotoxic T Lymphocytes ◽  
Cd8 T Cell ◽  
Cell Recognition ◽  
Gram Negative ◽  
T Cell Recognition ◽  
Histocompatibility Complex ◽  
Infected Cells ◽  
Bacterial Porins ◽  
Ompc Porin

ABSTRACT We report the identification of two peptides from Salmonella OmpC porin that can bind to major histocompatibility complex class I Kb molecules and are targets of cytotoxic T lymphocytes from Salmonella-infected mice. These peptides are conserved in gram-negative bacterial porins and are the first Salmonella porin-specific epitopes described for possible CD8+-T-cell elimination of infected cells.

Cytotoxic T cell recognition of Epstein-Barr virus-infected B cells. II. Blocking studies with monoclonal antibodies to HLA determinants

1981 ◽  
Vol 11 (9) ◽  
pp. 694-699 ◽  
Author(s):  
Lesley E. Wallace ◽  
Denis J. Moss ◽  
Alan B. Rickinson ◽  
Andrew J. McMichael ◽  
M. Anthony Epstein
Keyword(s):  
Monoclonal Antibodies ◽  
T Cell ◽  
B Cells ◽  
Epstein Barr Virus ◽  
Cytotoxic T Cell ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Barr Virus ◽  
Epstein Barr
Sign in / Sign up

Export Citation Format

Share Document