Nitric oxide-mediated suppression of T cell responses duringTrypanosoma brucei infection: soluble trypanosome products and interferon-γ are synergistic inducers of nitric oxide synthase

1996 ◽  
Vol 26 (3) ◽  
pp. 539-543 ◽  
Author(s):  
Jeremy M. Sternberg ◽  
Neil A. Mabbott
Keyword(s):  
Nitric Oxide ◽  
T Cell ◽  
Nitric Oxide Synthase ◽  
T Cell Responses ◽  
Interferon Γ ◽  
Cell Responses ◽  
Oxide Synthase

scholarly journals Interferon-γ-producing Tumor Induces Host Tumor-specific T Cell Responses

1993 ◽  
Vol 84 (6) ◽  
pp. 689-696 ◽  
Author(s):  
Yasufumi Teramura ◽  
Yoshihiko Watanabe ◽  
Norimichi Kan ◽  
Tohru Masuda ◽  
Kagemasa Kuribayashi
Keyword(s):  
T Cell ◽  
T Cell Responses ◽  
Interferon Γ ◽  
Cell Responses

Nitric oxide-producing CD11b+Ly-6G(Gr-1)+CD31(ER-MP12)+cells in the spleen of cyclophosphamide–treated mice: implications for T-cell responses in immunosuppressed mice

Blood ◽  
2000 ◽  
Vol 95 (1) ◽  
pp. 212-220 ◽  
Author(s):  
Iñigo Angulo ◽  
Federico Gómez de las Heras ◽  
José F. Garcı́a-Bustos ◽  
Domingo Gargallo ◽  
M. Angeles Muñoz-Fernández ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
T Cell ◽  
T Cell Responses ◽  
T Cell Proliferation ◽  
Intensive Chemotherapy ◽  
Suppressive Activity ◽  
Cell Responses ◽  
Nos Inhibitors ◽  
Ifn Γ

Abstract During recovery from intensive chemotherapy with cyclophosphamide (CTX), mice suffer a severe but transitory impairment in spleen cell proliferation to T-cell mitogens (Con A or anti-CD3 plus IL-2). Although CTX treatment reduced spleen T-cell cellularity, this cannot fully account for T-cell unresponsiveness. The results showed that CTX induces the colonization of spleen by an immature myeloid CD11b+Ly-6G+CD31+ population. Its presence closely correlated with the maximum inhibition of T-cell proliferation. Moreover, this suppressive activity was dependent on nitric oxide (NO) production in cultures since (1) higher amounts of nitric oxide and inducible nitric oxide synthase (iNOS) mRNA were produced in CTX spleen cells (CTX-SC) than in control splenocyte cultures and (2) NOS inhibitors greatly improved the proliferation of T lymphocytes. Nitric oxide production and suppressive activity were also dependent on endogenous interferon-γ (IFN-γ) production since anti–IFN-γ abrogated both effects. Finally, iNOS protein expression was restricted to a heterogeneous population of CD31+cells in which CD11b+Ly-6G+ cells were required to suppress T-cell proliferation. These results indicated that CTX might also cause immunosuppression by a mechanism involving the presence of immature myeloid cells with suppressor activity. This may have implications in clinical praxis since inappropriate immunotherapies in patients treated with intensive chemotherapy could lead to deleterious T-cell responses. (Blood. 2000;95:212-220)

scholarly journals αβ T Cell Receptor-positive Cells and Interferon-γ, but not Inducible Nitric Oxide Synthase, Are Critical for Granuloma Necrosis in a Mouse Model of Mycobacteria-induced Pulmonary Immunopathology

2001 ◽  
Vol 194 (12) ◽  
pp. 1847-1859 ◽  
Author(s):  
Stefan Ehlers ◽  
Jochen Benini ◽  
Heinz-Dieter Held ◽  
Christiane Roeck ◽  
Gottfried Alber ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
T Cell ◽  
Nitric Oxide Synthase ◽  
T Cell Receptor ◽  
Inducible Nitric Oxide Synthase ◽  
Bacterial Load ◽  
Cell Receptor ◽  
Ifn Γ ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The immunological basis of tuberculin-induced necrosis, known for more than a century as “Koch's phenomenon,” remains poorly understood. Aerosol infection in mice with the highly virulent Mycobacterium avium strain TMC724 causes progressive pulmonary pathology strongly resembling caseating necrosis in human patients with tuberculosis. To identify the cellular and molecular mediators causing this pathology, we infected C57BL/6 mice and mice selectively deficient in recombinase activating gene (RAG)-1, αβ T cell receptor (TCR), γδ TCR, CD4, CD8, β2-microglobulin, interferon (IFN)-γ, interleukin (IL)-10, IL-12p35, IL-12p35/p40, or iNOS with M. avium by aerosol and compared bacterial multiplication, histopathology, and respiratory physiology in these mice. The bacterial load in the lung was similarly high in all mouse groups. Pulmonary compliance, as a surrogate marker for granulomatous infiltrations in the lung, deteriorated to a similar extent in all groups of mice, except in αβ TCR-knockout (KO) and IL-12–KO mice in which compliance was higher, and in IFN-γ and inducible nitric oxide synthase–KO mice in which compliance was reduced faster. Progressive caseation of pulmonary granulomas never occurred in αβ TCR-KO, IL-12–KO, and IFN-γ–KO mice and was reduced in CD4-KO mice. In summary, αβ TCR+ cells and IFN-γ are essential for the development of mycobacteria-induced pulmonary caseous necrosis. In contrast, high mycobacterial load and extensive granulomatous infiltration per se are not sufficient to cause caseation, nor is granuloma necrosis linked to the induction of nitric oxide.

scholarly journals Modulation of human t cell responses by nitric oxide and its derivative,s-nitrosoglutathione

1993 ◽  
Vol 36 (10) ◽  
pp. 1414-1422 ◽  
Author(s):  
Parvin F. Merryman ◽  
Robert M. Clancy ◽  
Xiao Yuen He ◽  
Steven B. Abramson
Keyword(s):  
Nitric Oxide ◽  
T Cell ◽  
T Cell Responses ◽  
Cell Responses ◽  
Human T Cell
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