IL-17 attenuates the anti-apoptotic effects of GM-CSF in human neutrophils

Dragon, Stéphane; Saffar, Arash S.; Shan, Lianyu; Gounni, Abdelilah Soussi

doi:10.1016/j.molimm.2007.04.027

Cited by 61 publications

(59 citation statements)

References 38 publications

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“…In addition, both IL-23 and IL-17 promote expression of matrix metalloproteinase-9 (MMP-9) function while IL-17 alone promotes myeloperoxidase (MPO) activity. Zelante et al [5] also mention that addition of IL-23 or IL-17 resulted in reduced apoptosis, which has recently been reported for IL-17 [12]. These changes in neutrophil function and survival resulting from exposure to IL-23 or IL-17 may reconcile the data shown here with that from the IL-17ARKO mouse [7].…”

supporting

confidence: 77%

IL‐23 and IL‐17 have a multi‐faceted largely negative role in fungal infection

Cooper

2007

Eur J Immunol

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The role of IL-23 and IL-17 in the response to fungal infection has been the focus of recent reports. In this issue of the European Journal of Immunology there is an article that reports an important role for IL-23 and IL-17 in limiting fungal control, promoting neutrophillic inflammation and regulating the killing activity of neutrophils. In the fungal model it appears that IL-23 and IL-17 are counter-productive for protection.

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supporting

confidence: 77%

IL‐23 and IL‐17 have a multi‐faceted largely negative role in fungal infection

Cooper

2007

Eur J Immunol

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“…4). It has also been suggested that IL-17 may have a regulatory function limiting the accumulation and or activity of neutrophils during inflammation, by attenuating the anti-apoptotic effect of inflammatory cytokines [86]. IL-17R-defective mice had reduced CXC chemokine production, neutrophil recruitment and increased bacterial load and mortality following challenge with K. pneumoniae [13].…”

Section: Role Of Il-17-secreting T Cells In Infectionmentioning

confidence: 99%

Induction, function and regulation of IL‐17‐producing T cells

2008

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Recent reports have provided convincing evidence that IL-17-producing T cells play a key role in the pathogenesis of organ-specific autoimmune diseases, a function previously attributed exclusively to IFN-c-secreting Th1 cells. Furthermore, it appears that IL-17-producing T cells can also function with Th1 cells to mediate protective immunity to pathogens. Although much of the focus has been on IL-17-secreting CD4 1 T cells, termed The main function of IL-17-secreting T cells is to mediate inflammation, by stimulating production of inflammatory cytokines, such as TNF-a, IL-1b and IL-6, and inflammatory chemokines that promote the recruitment of neutrophils and macrophages.Key words: Autoimmunity . IL-17 . Infection . Inflammation IntroductionMore than 20 years ago Mosmann and Coffman reported that distinct CD4 1 T-cell subtypes, termed Th1 and Th2 cells, could be distinguished on the basis of cytokine secretion and function [1]. The Th1-Th2 model provided a useful but simplistic basis for our understanding of the mechanisms of immunity to infection and also attempted to explain the role of T cells in the pathogenesis of autoimmunity and allergy/asthma. The original hypothesis was that IFN-g-secreting CD4 1 cells mediated protective immunity to intracellular pathogens by promoting macrophage activation and stimulating production of complement fixing and virus neutralizing antibodies, but also promoted inflammatory responses and mediated the pathology in certain autoimmune diseases. In contrast, CD4 1 T cells that secreted IL-4, IL-5, IL-10 and IL-13 were considered to be the main helper T cells providing help for B-cell production of antibody, especially IgG1 in mice, and mediated protective immunity to extracellular pathogens. These Th2 cells were also anti-inflammatory, controlling Th1 responses, but at the same time mediated allergic reactions and had an inflammatory and pathological role in asthma.The identification of additional T-cell subtypes has led to a shift in the Th1-Th2 paradigm and has helped to explain some anomalies in the original model. In the mid 1990s suppressor T cells were re-discovered as Treg cells and were shown to have a major role in controlling immune responses to self-antigens, thereby preventing autoimmunity. Furthermore, these cells rather than the reciprocal Th1 or Th2 populations were shown to be the major regulator of effector T cells, functioning to maintain self-tolerance, prevent autoimmunity and limit collateral damage during immune responses to pathogens [2,3].There were a number of other observations which could not be explained on the basis of the two Th1 and Th2 subtypes. Mini-ReviewDespite the assumption that Th1 cells mediated autoimmunity, mice deficient in IFN-g or IFN-g receptors were found to have increased susceptibility to EAE and collagen-induced arthritis (CIA) [4,5]. Furthermore, EAE was exacerbated in mice deficient in the Th1 polarizing cytokine, 7]. It was then discovered that mice deficient in the novel IL-12 family member, IL-23 were resistant to EAE [6]....

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“…Subcutaneous injection of IL-17A into mice causes neutrophilia, which occurs by acceleration of neutrophil formation from committed progenitors and by enhanced chemotaxis [37,38]. In addition, IL-17A is able to directly inhibit apoptosis of neutrophils in inflamed tissues [39]. IL-17A also enhances angiogenesis [40] and mediates tissue remodeling by stimulating the production of angiogenic factors and matrix metalloproteases [41].…”

Section: Th17 Effector Cytokines: Il-17a Il-22 and Il-21mentioning

confidence: 99%

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

Fitch¹,

Harper²,

Skorcheva³

et al. 2007

Curr Rheumatol Rep

347

260

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T helper (Th) 17 cells, a novel T-cell subset, have been implicated in the pathogenesis of psoriasis and other autoimmune inflammatory diseases. Interleukin (IL)-23 stimulates survival and proliferation of Th17 cells, and thus serves as a key master cytokine regulator for these diseases. In psoriasis, IL-23 is overproduced by dendritic cells and keratinocytes, and this cytokine stimulates Th17 cells within dermis to make IL-17A and IL-22. IL-22, in particular, drives keratinocyte hyperproliferation in psoriasis. Future targeting of these key cytokines is likely to lead to dramatic clinical improvement in patients with psoriasis. This review focuses on the numerous recent studies on the roles of IL-23 and Th17 cells in the pathogenesis of psoriasis.

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IL-17 attenuates the anti-apoptotic effects of GM-CSF in human neutrophils

Cited by 61 publications

References 38 publications

IL‐23 and IL‐17 have a multi‐faceted largely negative role in fungal infection

IL‐23 and IL‐17 have a multi‐faceted largely negative role in fungal infection

Induction, function and regulation of IL‐17‐producing T cells

Pathophysiology of psoriasis: Recent advances on IL-23 and Th17 cytokines

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