scholarly journals Corrigendum: IL-2 Restores T-Cell Dysfunction Induced by Persistent Mycobacterium tuberculosis Antigen Stimulation

2020 ◽  
Vol 11 ◽  
Author(s):  
Xun Liu ◽  
Fei Li ◽  
Hongxia Niu ◽  
Lan Ma ◽  
Jianzhu Chen ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Antigen Stimulation ◽  
Cell Dysfunction ◽  
Tuberculosis Antigen ◽  
Mycobacterium Tuberculosis Antigen ◽  
T Cell Dysfunction

scholarly journals Compromised Metabolic Reprogramming Is an Early Indicator of CD8+ T Cell Dysfunction during Chronic Mycobacterium tuberculosis Infection

Cell Reports ◽  
2019 ◽  
Vol 29 (11) ◽  
pp. 3564-3579.e5 ◽  
Author(s):  
Shannon L. Russell ◽  
Dirk A. Lamprecht ◽  
Tawanda Mandizvo ◽  
Terrence T. Jones ◽  
Vanessa Naidoo ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Cd8 T Cell ◽  
Metabolic Reprogramming ◽  
Tuberculosis Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Early Indicator ◽  
Cell Dysfunction ◽  
T Cell Dysfunction

scholarly journals A Direct Role for the CD1b Endogenous Spacer in the Recognition of a Mycobacterium tuberculosis Antigen by T-Cell Receptors

2020 ◽  
Vol 11 ◽  
Author(s):  
Frank Camacho ◽  
Ernesto Moreno ◽  
Luis F. Garcia-Alles ◽  
Glay Chinea Santiago ◽  
Martine Gilleron ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
T Cell Receptors ◽  
Direct Role ◽  
Cell Receptors ◽  
Tuberculosis Antigen ◽  
Mycobacterium Tuberculosis Antigen

scholarly journals Phagosomal Processing of Mycobacterium tuberculosis Antigen 85B Is Modulated Independently of Mycobacterial Viability and Phagosome Maturation

2005 ◽  
Vol 73 (2) ◽  
pp. 1097-1105 ◽  
Author(s):  
Lakshmi Ramachandra ◽  
Jamie L. Smialek ◽  
Sam S. Shank ◽  
Marilyn Convery ◽  
W. Henry Boom ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
T Cell ◽  
Hybridoma Cells ◽  
Phagosome Maturation ◽  
Radiation Processing ◽  
Murine Bone Marrow ◽  
Mhc Ii ◽  
Tuberculosis Antigen ◽  
Class Ii Mhc ◽  
Mycobacterium Tuberculosis Antigen

ABSTRACT Control of Mycobacterium tuberculosis infection requires CD4 T-cell responses and major histocompatibility complex class II (MHC-II) processing of M. tuberculosis antigens (Ags). We have previously demonstrated that macrophages process heat-killed (HK) M. tuberculosis more efficiently than live M. tuberculosis. These observations suggested that live M. tuberculosis may inhibit Ag processing by inhibiting phagosome maturation or that HK M. tuberculosis may be less resistant to Ag processing. In the present study we examined the correlation between M. tuberculosis viability and phagosome maturation and efficiency of Ag processing. Since heat treatment could render M. tuberculosis Ags more accessible to proteolysis, M. tuberculosis was additionally killed by antibiotic treatment and radiation. Processing of HK, live, radiation-killed (RadK), or rifampin-killed (RifK) M. tuberculosis in activated murine bone marrow macrophages was examined by using an I-Ab-restricted T-cell hybridoma cell line (BB7) that recognizes an epitope derived from Ag 85B. Macrophages processed HK M. tuberculosis more rapidly and efficiently than they processed live, RadK, or RifK M. tuberculosis. Live, RadK, and RifK M. tuberculosis cells were processed with similar efficiencies for presentation to BB7 T hybridoma cells. Furthermore, phagosomes containing live or RadK M. tuberculosis expressed fewer M. tuberculosis peptide-MHC-II complexes than phagosomes containing HK M. tuberculosis expressed. Since only live M. tuberculosis was able to prevent acidification of the phagosome, our results suggest that regulation of phagosome maturation does not explain the differences in processing of different forms of M. tuberculosis. These findings suggest that the mechanisms used by M. tuberculosis to inhibit phagosomal maturation differ from the mechanisms involved in modulating phagosome Ag processing.

scholarly journals Upregulation of Tim-3 and PD-1 expression is associated with tumor antigen–specific CD8+ T cell dysfunction in melanoma patients

2010 ◽  
Vol 207 (10) ◽  
pp. 2175-2186 ◽  
Author(s):  
Julien Fourcade ◽  
Zhaojun Sun ◽  
Mourad Benallaoua ◽  
Philippe Guillaume ◽  
Immanuel F. Luescher ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cd8 T Cells ◽  
Tumor Antigen ◽  
Cytokine Production ◽  
Cd8 T Cell ◽  
Advanced Melanoma ◽  
Antigen Stimulation ◽  
Cell Dysfunction ◽  
T Cell Dysfunction

The paradoxical coexistence of spontaneous tumor antigen–specific immune responses with progressive disease in cancer patients furthers the need to dissect the molecular pathways involved in tumor-induced T cell dysfunction. In patients with advanced melanoma, we have previously shown that the cancer-germline antigen NY-ESO-1 stimulates spontaneous NY-ESO-1–specific CD8+ T cells that up-regulate PD-1 expression. We also observed that PD-1 regulates NY-ESO-1–specific CD8+ T cell expansion upon chronic antigen stimulation. In the present study, we show that a fraction of PD-1+ NY-ESO-1–specific CD8+ T cells in patients with advanced melanoma up-regulates Tim-3 expression and that Tim-3+PD-1+ NY-ESO-1–specific CD8+ T cells are more dysfunctional than Tim-3−PD-1+ and Tim-3−PD-1− NY-ESO-1–specific CD8+ T cells, producing less IFN-γ, TNF, and IL-2. Tim-3–Tim-3L blockade enhanced cytokine production by NY-ESO-1–specific CD8+ T cells upon short ex vivo stimulation with cognate peptide, thus enhancing their functional capacity. In addition, Tim-3–Tim-3L blockade enhanced cytokine production and proliferation of NY-ESO-1–specific CD8+ T cells upon prolonged antigen stimulation and acted in synergy with PD-1–PD-L1 blockade. Collectively, our findings support the use of Tim-3–Tim-3L blockade together with PD-1–PD-L1 blockade to reverse tumor-induced T cell exhaustion/dysfunction in patients with advanced melanoma.

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