T-Cell Responses during<i>Trypanosoma brucei</i>Infections in Mice Deficient in Inducible Nitric Oxide Synthase

Millar, Amanda E.; Sternberg, Jerry; McSharry, C; Wei, Xiaoguang; Liew, Foo Y.; Turner, C. Michael R.

doi:10.1128/iai.67.7.3334-3338.1999

Cited by 48 publications

(16 citation statements)

References 28 publications

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“…Mice lacking inducible NO synthase showed increased numbers of CD4 T cells after infection with Trypanosome brucei. However, the level of apoptosis of these CD4 T cells was not measured (29).…”

Section: Discussionmentioning

confidence: 99%

Interferon γ Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells

Dalton

Haynes

Chu

et al. 2000

The Journal of Experimental Medicine

310

266

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In Mycobacterium bovis Bacille Calmette-Guérin (BCG)-infected wild-type mice, there was a large expansion of an activated (CD44hi) splenic CD4 T cell population followed by a rapid contraction of this population to normal numbers. Contraction of the activated CD4 T cell population in wild-type mice was associated with increased apoptosis of activated CD4 T cells. In BCG-infected interferon (IFN)-γ knockout (KO) mice, the activated CD4 T cell population did not undergo apoptosis. These mice accumulated large numbers of CD4+CD44hi T cells that were responsive to mycobacterial antigens. Addition of IFN-γ to cultured splenocytes from BCG-infected IFN-γ KO mice induced apoptosis of activated CD4 T cells. IFN-γ–mediated apoptosis was abolished by depleting adherent cells or Mac-1+ spleen cells or by inhibiting nitric oxide synthase. Thus, IFN-γ is essential to a regulatory mechanism that eliminates activated CD4 T cells and maintains CD4 T cell homeostasis during an immune response.

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Section: Discussionmentioning

confidence: 99%

Interferon γ Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells

Dalton

Haynes

Chu

et al. 2000

The Journal of Experimental Medicine

310

266

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“…Single-cell spleen suspensions were prepared at 0, 4,5,6,7,8,9,10,14,17,21,24 and 28 days post-infection (dpi) as previously described. 13 Unless otherwise stated, cell suspensions were re-suspended in 0.05% FBS BD FACSFlow Sheath Fluid.…”

Section: Cell Isolation and Flow Cytometry Assaymentioning

confidence: 99%

Trypanosoma brucei brucei causes a rapid and persistent influx of neutrophils in the spleen of infected mice

Deleeuw

Phạm

Poorter

et al. 2019

Parasite Immunology

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Trypanosomosis is a chronic parasitic infection, affecting both humans and livestock. A common hallmark of experimental murine infections is the occurrence of inflammation and the associated remodelling of the spleen compartment. The latter involves the depletion of several lymphocyte populations, the induction of T‐cell‐mediated immune suppression, and the activation of monocyte/macrophage cell populations. Here, we show that in experimental T b brucei infections in mice, these changes are accompanied by the alteration of the spleen neutrophil compartment. Indeed, mature neutrophils are rapidly recruited to the spleen, and cell numbers remain elevated during the entire infection. Following the second peak of parasitemia, the neutrophil cell influx coincides with the rapid reduction of splenic marginal zone (MZ)B and follicular (Fo)B cells, as well as CD8+ T and NK1.1+ cells, the latter encompassing both natural killer (NK) and natural killer T (NKT) cells. This report is the first to show a comprehensive overview of all alterations in spleen cell populations, measured with short intervals throughout the entire course of an experimental T b brucei infection. These data provide new insights into the dynamic interlinked changes in spleen cell numbers associated with trypanosomosis‐associated immunopathology.

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“…The molecular bases for immunosuppression and the suppressor cell effect were revealed in later studies showing that NO, PGE 2 and/or TNF‐α were the primary suppressor effector molecules (69–77). The primary biological effect of suppressor macrophages and their products was shown to be inhibition of T‐cell proliferative responses to VSG and other trypanosome antigens, with relatively little impact on cytokine secretion (70,71).…”

Section: Regulation Of T Lymphocyte Responsesmentioning

confidence: 99%

Regulation of innate and acquired immunity in African trypanosomiasis

Mansfield

Paulnock

2005

Parasite Immunology

109

121

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African trypanosomes are well known for their ability to avoid immune elimination by switching the immunodominant variant surface glycoprotein (VSG) coat during infection. However, antigenic variation is only one of several means by which trypanosomes manipulate the immune system of their hosts. In this article, the role of parasite factors such as GPI anchor residues of the shed VSG molecule and the release of CpG DNA, in addition to host factors such as IFN-gamma, in regulating key aspects of innate and acquired immunity during infection is examined. The biological relevance of these immunoregulatory events is discussed in the context of host and parasite survival.

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T-Cell Responses duringTrypanosoma bruceiInfections in Mice Deficient in Inducible Nitric Oxide Synthase

Cited by 48 publications

References 28 publications

Interferon γ Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells

Interferon γ Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells

Trypanosoma brucei brucei causes a rapid and persistent influx of neutrophils in the spleen of infected mice

Regulation of innate and acquired immunity in African trypanosomiasis

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