Protective Role of Naturally Occurring Interleukin-17A-Producing γδ T Cells in the Lung at the Early Stage of Systemic Candidiasis in Mice

Dejima, Takashi; Shibata, Kensuke; Yamada, Hisakata; Hara, Hiromitsu; Iwakura, Yoichiro; Naito, Seiji; Yoshikai, Yasunobu

doi:10.1128/iai.05799-11

Cited by 76 publications

(77 citation statements)

References 53 publications

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“…However, we observed that TCR-d and TAP1 deficiency, but not MHCII deficiency, also affected early Brucella control in the lungs, suggesting that these cells could be a potential source of IL-17A in our model. In keeping with this observation, IL-17 production by g/d T cells was reported in a Brucella model (65) and in several other pulmonary infectious models (66)(67)(68).…”

Section: Discussionmentioning

confidence: 52%

Identification of Immune Effectors Essential to the Control of Primary and Secondary Intranasal Infection with Brucella melitensis in Mice

Mambres

Machelart

Potemberg

et al. 2016

The Journal of Immunology

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The mucosal immune system represents the first line of defense against Brucella infection in nature. We used genetically deficient mice to identify the lymphocytes and signaling pathways implicated in the control of primary and secondary intranasal infection with B. melitensis. Our analysis of primary infection demonstrated that the effectors implicated differ at the early and late stages and are dependent on the organ. TCR-δ, TAP1, and IL-17RA deficiency specifically affects early control of Brucella in the lungs, whereas MHC class II (MHCII) and IFN-γR deficiency impairs late control in the lungs, spleen, and liver. Interestingly, IL-12p35−/− mice display enhanced Brucella growth in the spleen but not in the lungs or liver. Secondary intranasal infections are efficiently contained in the lung. In contrast to an i.p. infectious model, in which IL-12p35, MHCII, and B cells are strictly required for the control of secondary infection, we observed that only TCR-β deficiency or simultaneous neutralization of IL-12p35– and IL-17A–dependent pathways impairs the memory protective response against a secondary intranasal infection. Protection is not affected by TCR-δ, MHCII, TAP1, B cell, IL-17RA, or IL-12p35 deficiency, suggesting that CD4+ and CD8+ α/β+ T cells are sufficient to mount a protective immune response and that an IL-17A–mediated response can compensate for the partial deficiency of an IFN-γ–mediated response to control a Brucella challenge. These findings demonstrate that the nature of the protective memory response depends closely on the route of infection and highlights the role of IFN-γ–and IL-17RA–mediated responses in the control of mucosal infection by Brucella.

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Section: Discussionmentioning

confidence: 52%

Identification of Immune Effectors Essential to the Control of Primary and Secondary Intranasal Infection with Brucella melitensis in Mice

Mambres

Machelart

Potemberg

et al. 2016

The Journal of Immunology

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“…γδ 17 cells are observed in lungs after systemic C. albicans infection, and both Il17 −/− and Tcrd −/− mice are defective in neutrophil recruitment and fungal clearance 84. Interleukin‐17 is produced in tongue‐resident γδ T cells as well as CD3 + CD4 + CD44 hi TCR‐ β + CCR6 + natural Th17 cells within 1–2 days after oral C. albicans infection 85.…”

Section: γδ17 Cells In Pathogen Clearancementioning

confidence: 99%

Interleukin‐17‐producing γδ T (γδ17) cells in inflammatory diseases

Akitsu

Iwakura

2018

Immunology

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SummaryInterleukin‐17 (IL‐17) is a pro‐inflammatory cytokine and is involved in the development of many diseases. Recent studies have revealed that IL‐17‐producing γδ T cells (γδ17 cells) in addition to IL‐17‐producing CD4+ T cells [T helper type 17 (Th17) cells] are often the main producers of IL‐17 in mouse models of inflammatory diseases. γδ T cells are functionally committed during intra‐thymic differentiation. γδ thymocytes capable of producing IL‐17, which express the transcription factor retinoic‐acid‐receptor‐related orphan receptor γt and the signature cytokine receptor IL‐23R, leave the thymus, and produce IL‐17 rapidly by the stimulation with IL‐1β and IL‐23 in the periphery. Therefore, γδ17 cells play important roles in the early phase of host defence against pathogens and in inflammatory diseases. γδ T cells that can produce IL‐17 are also increased in the skin of patients with psoriasis and in peripheral blood of patients with ankylosing sclerosis. Indeed, the therapy targeting IL‐17 has been approved or is in clinical trials, and proved to be very efficient to treat psoriasis, psoriatic arthritis and ankylosing sclerosis. In this review, we discuss recent knowledge about the pathophysiological function of γδ17 cells in infection and inflammatory diseases and therapeutic advances targeting IL‐17.

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“…Recently, it was found that IL-17A production by ␥␦ T cells rather than CD4 ϩ ␣␤ T cells plays an important role in the immune response to pulmonary Mycobacterium bovis Bacillus Calmette-Guérin (BCG) infection as well as in BCG-induced lung granuloma formation (13)(14)(15). We have also reported the importance of IL-17A-producing ␥␦ T cells in other models of infection of mice with Escherichia coli, Candia albicans, or BCG, which are involved in the neutrophil-mediated clearance of the pathogens or tumor cells (16)(17)(18). These findings suggest the hypothesis that a novel host defense mechanism mediated by the "innate" IL-17A-producing ␥␦ T cells is acting in innate immunity and initiating an inflammatory response following a microbe invasion.…”

mentioning

confidence: 97%

CD30 Is Required for Activation of a Unique Subset of Interleukin-17A-Producing γδ T Cells in Innate Immunity against Mycobacterium bovis Bacillus Calmette-Guérin Infection

et al. 2013

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Protective Role of Naturally Occurring Interleukin-17A-Producing γδ T Cells in the Lung at the Early Stage of Systemic Candidiasis in Mice

Cited by 76 publications

References 53 publications

Identification of Immune Effectors Essential to the Control of Primary and Secondary Intranasal Infection with Brucella melitensis in Mice

Identification of Immune Effectors Essential to the Control of Primary and Secondary Intranasal Infection with Brucella melitensis in Mice

Interleukin‐17‐producing γδ T (γδ17) cells in inflammatory diseases

CD30 Is Required for Activation of a Unique Subset of Interleukin-17A-Producing γδ T Cells in Innate Immunity against Mycobacterium bovis Bacillus Calmette-Guérin Infection

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