Regulatory T Cells Resist Virus Infection-Induced Apoptosis

Wun-Yue, Jenny; Kraft, Anke; Selin, Liisa K.; Welsh, Raymond M.

doi:10.1128/jvi.02245-14

Cited by 15 publications

(13 citation statements)

References 63 publications

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“…The large number of HLA-A2/M1-specific clonotypes contributes to the overall memory T cell pool, enhancing the opportunity for protective heterologous immunity now recognized to be an important aspect of immune maturation 50,51 . A large pool of TCR clonotypes responding to HLA-A2/M1 could provide increased resistance to viral drift, although the xRS/A-containing JM22 TCR recently has been shown to be able to recognize M1 variants from circulating IAV strains 52 .…”

Section: Discussionmentioning

confidence: 99%

Broad TCR repertoire and diverse structural solutions for recognition of an immunodominant CD8+ T cell epitope

Song

Gil

Mishra

et al. 2017

Nat Struct Mol Biol

121

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A keystone of antiviral immunity is CD8 T-cell recognition of viral peptides bound to MHC-I proteins. The recognition mode of individual T cell receptors (TCRs) has been studied in some detail, but how TCR variation functions in providing a robust response to viral antigen is unclear. The influenza M1 epitope is an immunodominant target of CD8 T cells helping to control influenza in HLA-A2+ individuals. Here, we show that many distinct TCRs are used by CD8 T cells to recognize HLA-A2/M1, encoding different structural solutions to the problem of specifically recognizing a relatively featureless peptide antigen. The vast majority of responding TCRs target small clefts between peptide and MHC. These broad repertoires lead to plasticity in antigen recognition and protection against T cell clonal loss and viral escape.

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Section: Discussionmentioning

confidence: 99%

Broad TCR repertoire and diverse structural solutions for recognition of an immunodominant CD8+ T cell epitope

Song

Gil

Mishra

et al. 2017

Nat Struct Mol Biol

121

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“…The pleiotropic effects of type I IFNs on T cells can vary from beneficial (promoting their expansion) to detrimental (inhibiting their proliferation and driving apoptosis), depending on timing and prior antigen experience (Welsh and others 2012 ; Urban and Welsh 2014 ). T cell subsets are also differentially affected, for example, regulatory T cells have recently been shown to be relatively resistant to the apoptosis-inducing effects of type I IFN (Che and others 2014 ). Overall, early in LCMV infection, type I IFN-induced antiviral factors aid the control of viral replication (Muller and others 1994 ).…”

Section: Viral Infectionmentioning

confidence: 99%

Disease-Promoting Effects of Type I Interferons in Viral, Bacterial, and Coinfections

Davidson¹,

Maini²,

Wack³

2015

Journal of Interferon & Cytokine Research

172

162

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While type I interferons (IFNs) are universally acknowledged for their antiviral and immunostimulatory functions, there is increasing appreciation of the detrimental effects of inappropriate, excessive, or mistimed type I IFN responses in viral and bacterial infections. The underlying mechanisms by which type I IFNs promote susceptibility or severity include direct tissue damage by apoptosis induction or suppression of proliferation in tissue cells, immunopathology due to excessive inflammation, and cell death induced by TRAIL- and Fas-expressing immune cells, as well as immunosuppression through IL-10, IL-27, PD-L1, IL-1Ra, and other regulatory molecules that antagonize the induction or action of IL-1, IL-12, IL-17, IFN-γ, KC, and other effectors of the immune response. Bacterial superinfections following influenza infection are a prominent example of a situation where type I IFNs can misdirect the immune response. This review discusses current understanding of the parameters of signal strength, duration, timing, location, and cellular recipients that determine whether type I IFNs have beneficial or detrimental effects in infection.

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“…These two subsets share a common precursor, but their functions are quite different . Tregs are characterized by the expression of forkhead box protein 3 (FoxP3) and, in viral infection, play an important role in maintaining immune homoeostasis by controlling exaggerated and destructive inflammations . On the other hand, inhibition of virus‐specific T cell responses by the Tregs depresses antiviral immune response facilitating viral persistence and disease progression.…”

Section: Introductionmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection. How to cite this article: Wan Z, Zhou Z, Liu Y, et al. Regulatory T cells and T helper 17 cells in viral infection. Scand J Immunol. 2020;91:e12873.

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Regulatory T Cells Resist Virus Infection-Induced Apoptosis

Cited by 15 publications

References 63 publications

Broad TCR repertoire and diverse structural solutions for recognition of an immunodominant CD8+ T cell epitope

Broad TCR repertoire and diverse structural solutions for recognition of an immunodominant CD8+ T cell epitope

Disease-Promoting Effects of Type I Interferons in Viral, Bacterial, and Coinfections

Regulatory T cells and T helper 17 cells in viral infection

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