Regulatory T Cells Selectively Preserve Immune Privilege of Self-Antigens during Viral Central Nervous System Infection

Cervantes-Barragán, Luisa; Firner, Sonja; Bechmann, Ingo; Waisman, Ari; Lahl, Katharina; Sparwasser, Tim; Thiel, Volker; Ludewig, Burkhard

doi:10.4049/jimmunol.1102422

Cited by 42 publications

(39 citation statements)

References 46 publications

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“…It also not excluded that IP-10 production subsequent to the early peak of IFN-I is fueled by other factors, such as IFN-γ or TNF-α [41]. IP-10 is the ligand of CXCR3, which is expressed on many cells (activated T cells, Th1 cells, Treg cells, plasmacytoid dendritic cells, monocytes, NK cells) and is implicated in the recruitment of CXCR3 + cells to lymph nodes [42], [43], [44]. Events in lymph nodes might have a particular impact on immunodeficiency [45].…”

Section: Discussionmentioning

confidence: 99%

Acute Plasma Biomarkers of T Cell Activation Set-Point Levels and of Disease Progression in HIV-1 Infection

et al. 2012

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T cell activation levels, viral load and CD4+ T cell counts at early stages of HIV-1 infection are predictive of the rate of progression towards AIDS. We evaluated whether the inflammatory profile during primary HIV-1 infection is predictive of the virological and immunological set-points and of disease progression. We quantified 28 plasma proteins during acute and post-acute HIV-1 infection in individuals with known disease progression profiles. Forty-six untreated patients, enrolled during primary HIV-1 infection, were categorized into rapid progressors, progressors and slow progressors according to their spontaneous progression profile over 42 months of follow-up. Already during primary infection, rapid progressors showed a higher number of increased plasma proteins than progressors or slow progressors. The plasma levels of TGF-β1 and IL-18 in primary HIV-1 infection were both positively associated with T cell activation level at set-point (6 months after acute infection) and together able to predict 74% of the T cell activation variation at set-point. Plasma IP-10 was positively and negatively associated with, respectively, T cell activation and CD4+ T cell counts at set-point and capable to predict 30% of the CD4+ T cell count variation at set-point. Moreover, plasma IP-10 levels during primary infection were predictive of rapid progression. In primary infection, IP-10 was an even better predictor of rapid disease progression than viremia or CD4+ T cell levels at this time point. The superior predictive capacity of IP-10 was confirmed in an independent group of 88 HIV-1 infected individuals. Altogether, this study shows that the inflammatory profile in primary HIV-1 infection is associated with T cell activation levels and CD4+ T cell counts at set-point. Plasma IP-10 levels were of strong predictive value for rapid disease progression. The data suggest IP-10 being an earlier marker of disease progression than CD4+ T cell counts or viremia levels.

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Section: Discussionmentioning

confidence: 99%

Acute Plasma Biomarkers of T Cell Activation Set-Point Levels and of Disease Progression in HIV-1 Infection

et al. 2012

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“…In addition, peripheral MHV infection correlated with induction of SR T cells detected within the spleen of chronically infected mice (Kyuwa et al, 1991). More recently, it was demonstrated that acute MHV-A59 infection supports peripheral proliferation and CNS recruitment of transferred T-cell receptor transgenic myelin-specific CD4 T cells (Cervantes-Barragan et al, 2012). Similarly, we showed that naïve myelin oligodendrocyte glycoprotein (MOG)-specific CD4 T cells transferred prior to JHMV infection proliferated in cervical lymph nodes (CLN) and migrate to the CNS (Savarin et al, 2015).…”

Section: Self Reactive Cd4 T Cell Response During Neurotropic Mhv mentioning

confidence: 99%

Viral-induced suppression of self-reactive T cells: Lessons from neurotropic coronavirus-induced demyelination

Savarin

Bergmann

2017

Journal of Neuroimmunology

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Genetic and environmental factors, i.e. infections, have been proposed to contribute to disease induction and relapsing events in multiple sclerosis (MS), an autoimmune demyelinating disease of the central nervous system (CNS). While research has mainly focused on virus associated autoimmune activation, less is known about prevention of autoimmunity, especially following resolving infections associated with CNS tissue damage. This review discusses novel insights on control of self-reactive (SR) T cells activated during neurotropic coronavirus-induced demyelination. A new concept is introduced that SR T cells can be dampened by distinct regulatory mechanisms in the periphery and the CNS, thereby preventing autoimmune disease.

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“…This concept is well-illustrated by the demyelinating disease that develops following infection with a neurotropic strain of murine hepatitis virus (MHV). Depletion of Treg cells in this context has little or no effect on the magnitude of the anti-viral immune response or viral clearance, but greatly exacerbates neurological pathology and the activation of myelin-specific T cells (142), indicating that at least in this case Treg cells are selectively modulating the activation and functional differentiation of self-reactive T cells.…”

Section: Critical Issues In Treg Cell Biologymentioning

confidence: 99%

Organ-Specific and Memory Treg Cells: Specificity, Development, Function, and Maintenance

2014

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Foxp3+ regulatory T cells (Treg cells) are essential for establishing and maintaining self-tolerance, and also inhibit immune responses to innocuous environmental antigens. Imbalances and dysfunction in Treg cells lead to a variety of immune-mediated diseases, as deficits in Treg cell function contribute to the development autoimmune disease and pathological tissue damage, whereas overabundance of Treg cells can promote chronic infection and tumorigenesis. Recent studies have highlighted the fact that Treg cells themselves are a diverse collection of phenotypically and functionally specialized populations, with distinct developmental origins, antigen-specificities, tissue-tropisms, and homeostatic requirements. The signals directing the differentiation of these populations, their specificities and the mechanisms by which they combine to promote organ-specific and systemic tolerance, and how they embody the emerging property of regulatory memory are the focus of this review.

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Regulatory T Cells Selectively Preserve Immune Privilege of Self-Antigens during Viral Central Nervous System Infection

Cited by 42 publications

References 46 publications

Acute Plasma Biomarkers of T Cell Activation Set-Point Levels and of Disease Progression in HIV-1 Infection

Acute Plasma Biomarkers of T Cell Activation Set-Point Levels and of Disease Progression in HIV-1 Infection

Viral-induced suppression of self-reactive T cells: Lessons from neurotropic coronavirus-induced demyelination

Organ-Specific and Memory Treg Cells: Specificity, Development, Function, and Maintenance

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