Expression of Toll-Like Receptor 2 on γδ T Cells Bearing Invariant Vγ6/Vδ1 Induced by<i>Escherichia coli</i>Infection in Mice

Mokuno, Yasuji; Matsuguchi, Tetsuya; Takano, Manabu; Nishimura, Hitoshi; Washizu, Junji; Ogawa, Tomohiko; Takeuchi, Osamu; Akira, Shizuo; Nimura, Yuji; Yoshikai, Yasunobu

doi:10.4049/jimmunol.165.2.931

Cited by 134 publications

(133 citation statements)

References 61 publications

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“…infection with E. coli (23)(24)(25)(26), we further examined the IL-17 production and neutrophil infiltration in V␦1 Ϫ/Ϫ mice. Although there was no difference in the number of ␥␦ T cells between naive V␦1 ϩ/Ϫ and V␦1 Ϫ/Ϫ mice, IL-17 production 6 h after i.p.…”

Section: ␥␦ T Cells Are Responsible For the Il-17 Production And Neutmentioning

confidence: 99%

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Resident Vδ1+ γδ T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production

Shibata

Yamada

Hara

et al. 2007

The Journal of Immunology

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440

410

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Neutrophils infiltrate the site of infection and play critical roles in host defense, especially against extracellular bacteria. In the present study, we found a rapid and transient production of IL-17 after i.p. infection with Escherichia coli, preceding the influx of neutrophils. Neutralization of IL-17 resulted in a reduced infiltration of neutrophils and an impaired bacterial clearance. Ex vivo intracellular cytokine flow cytometric analysis revealed that γδ T cell population was the major source of IL-17. Mice depleted of γδ T cells by mAb treatment or mice genetically lacking Vδ1 showed diminished IL-17 production and reduced neutrophil infiltration after E. coli infection, indicating an importance of Vδ1+ γδ T cells as the source of IL-17. It was further revealed that γδ T cells in the peritoneal cavity of naive mice produced IL-17 in response to IL-23, which was induced rapidly after E. coli infection in a TLR4 signaling-dependent manner. Thus, although γδ T cells are generally regarded as a part of early induced immune responses, which bridge innate and adaptive immune responses, our study demonstrated a novel role of γδ T cells as a first line of host defense controlling neutrophil-mediated innate immune responses.

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Section: ␥␦ T Cells Are Responsible For the Il-17 Production And Neutmentioning

confidence: 99%

“…infection with Escherichia coli (23)(24)(25)(26). Although it is well established that neutrophils are essential in bacterial clearance, roles of IL-17 in this model are unknown.…”

mentioning

confidence: 99%

Resident Vδ1+ γδ T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production

Shibata

Yamada

Hara

et al. 2007

The Journal of Immunology

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440

410

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“…Preparation and adoptive transfer of TCR gd T cells TCR Vg6 + gd T cells were prepared from Escherichia coli (E. coli)-infected peritoneal cavity (PEC) cells as reported previously (21,22), because E. coli-induced peritoneal TCR gd T cells consist exclusively of TCR Vg6 + gd T cells (21,22) and express IL-17A (23). TCR Vg4 + gd T cells were obtained from the lung infected i.…”

Section: Histopathologymentioning

confidence: 99%

Essential Role of IL-17A in the Formation of a Mycobacterial Infection-Induced Granuloma in the Lung

Yoshida

Umemura

Yahagi

et al. 2010

The Journal of Immunology

348

261

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Granulomas play an essential role in the sequestration and killing of mycobacteria in the lung; however, the mechanisms of their development and maturation are still not clearly understood. IL-17A is involved in mature granuloma formation in the mycobacteria-infected lung. Therefore, IL-17A gene-knockout (KO) mice fail to develop mature granulomas in the Mycobacterium bovis bacille Calmette-Guérin (BCG)-infected lung. This study analyzed the mechanism of IL-17A–dependent mature granuloma formation in the mycobacteria-infected lung. The IL-17A KO mice showed a normal level of nascent granuloma formation on day 14 but failed to develop mature granulomas on day 28 after the BCG infection in the lung. The observation implies that IL-17A is required for the maturation of granuloma from the nascent to mature stage. TCR γδ T cells expressing TCR Vγ4 or Vγ6 were identified as the major IL-17A–producing cells that resided in the BCG-induced lung granuloma. The adoptive transfer of the IL-17A–producing TCR γδ T cells reconstituted granuloma formation in the IL-17A KO mice. The expression of ICAM-1 and LFA-1, which are adhesion molecules important in granuloma formation, decreased in the lung of the BCG-infected IL-17A KO mice, and their expression was induced on BCG-infected macrophages in coculture with IL-17A–producing TCR γδ T cells. Furthermore, IL-17A KO mice showed not only an impaired mature granuloma formation, but also an impaired protective response to virulent Mycobacterium tuberculosis. Therefore, IL-17A produced by TCR γδ T cells plays a critical role in the prevention of M. tuberculosis infection through the induction of mature granuloma formation.

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“…Also, though it is widely accepted that γδ T cells recognize microbial nonpeptidic phosphorylated molecules [16][17][18] and alkylamines [19,20] in a TCRdependent manner, LPS has not, to our knowledge, been described as a TCR ligand. While we have not precisely determined the mechanism of LPS detection, transcripts encoding many TLRs and other pattern recognition proteins are readily detected in γδ T cells [15,[21][22][23][24][25]. Other groups have shown that TLR agonists have co-stimulatory effects in combination with TCR engagement on γδ T cells, similar in many respects to the priming effect described here [21,25].…”

Section: Discussionmentioning

confidence: 58%

Mucosal lymphatic-derived γδ T cells respond early to experimental Salmonella enterocolitis by increasing expression of IL-2Rα

Hedges

Buckner

Rask

et al. 2007

Cellular Immunology

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To better understand the roles of γδ T cells in mucosal infection, we utilized Salmonella enterica serovar Typhimurium (Salmonella serovar Typhimurium) infection in cattle as it closely approximates Salmonella serovar Typhimurium-induced enterocolitis in humans. Protein and gene expression in αβ and γδ T cells derived from lymphatic ducts draining the gut mucosa in Salmonella serovar Typhimurium infected calves were analyzed. In calves with enterocolitis, general gene expression trends in γδ T cells suggested subtle activation and innate response, whereas αβ T cells were relatively quiescent following Salmonella serovar Typhimurium infection. An increase in IL-2Rα expression on γδ T cells from infected calves and results from in vitro assays suggested that γδ T cells were primed by Salmonella serovar Typhimurium LPS to better respond to IL-2 and IL-15. Together with gene expression trends in vivo, these data support early priming activation of target tissue γδ T cells during Salmonella serovar Typhimurium infection.

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Expression of Toll-Like Receptor 2 on γδ T Cells Bearing Invariant Vγ6/Vδ1 Induced byEscherichia coliInfection in Mice

Cited by 134 publications

References 61 publications

Resident Vδ1+ γδ T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production

Resident Vδ1+ γδ T Cells Control Early Infiltration of Neutrophils after Escherichia coli Infection via IL-17 Production

Essential Role of IL-17A in the Formation of a Mycobacterial Infection-Induced Granuloma in the Lung

Mucosal lymphatic-derived γδ T cells respond early to experimental Salmonella enterocolitis by increasing expression of IL-2Rα

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