scholarly journals Two Types of Interleukin 17A–Producing γδ T Cells in Protection Against Pulmonary Infection WithKlebsiella pneumoniae

2016 ◽  
Vol 214 (11) ◽  
pp. 1752-1761 ◽  
Author(s):  
Tesshin Murakami ◽  
Shinya Hatano ◽  
Hisakata Yamada ◽  
Yoichiro Iwakura ◽  
Yasunobu Yoshikai
Immunology ◽  
2008 ◽  
Vol 125 (2) ◽  
pp. 170-177 ◽  
Author(s):  
Satoru Hamada ◽  
Masayuki Umemura ◽  
Takeru Shiono ◽  
Hiromitsu Hara ◽  
Kenji Kishihara ◽  
...  

2001 ◽  
Vol 69 (10) ◽  
pp. 6165-6171 ◽  
Author(s):  
Stanley Tam ◽  
Donald P. King ◽  
Blaine L. Beaman

ABSTRACT Previous studies have demonstrated that γδ T lymphocytes are important for host resistance to pulmonary infection of the murine lung by log-phase cells of Nocardia asteroides. To study the role of γδ T cells in nocardial interactions in the murine lung, C57BL/6J wild type and C57BL/6J-Tcrd (γδ T-cell knockout mice) were infected intranasally with log-phase cells of N. asteroidesGUH-2. At 3, 5, and 7 days after infection, the γδ T cells were quantified by multiparameter flow cytometry. At the same time, Gram and hematoxylin-eosin stains of paraffin sections were performed to monitor the host responses. The data showed that γδ T lymphocytes increased significantly within the lungs after intranasal infection, and the peak of this cellular increase occurred at 5 days. Furthermore, at this time, greater than 50% of the CD3 T-cell receptor (TCR)-positive (CD3+) cells were γδ TCR positive. Histological examination clearly showed divergent inflammatory responses in the lungs of wild-type mice compared to γδ T-cell knockout mice. The C57BL/6J-Tcrd mice were less capable of clearing the organism, and the polymorphonuclear leukocyte response lasted longer than in wild-type C57BL/6J mice. These results showed that γδ T cells were actively involved in modulating the innate host responses to murine pulmonary infection by N. asteroides.


2011 ◽  
Vol 79 (11) ◽  
pp. 4503-4510 ◽  
Author(s):  
Takashi Dejima ◽  
Kensuke Shibata ◽  
Hisakata Yamada ◽  
Hiromitsu Hara ◽  
Yoichiro Iwakura ◽  
...  

ABSTRACTInterleukin-17A (IL-17A)-producing γδ T cells differentiate in the fetal thymus and reside in the peripheral tissues, such as the lungs of naïve adult mice. We show here that naturally occurring γδ T cells play a protective role in the lung at a very early stage after systemic infection withCandida albicans.Selective depletion of neutrophils byin vivoadministration of anti-Ly6G monoclonal antibody (MAb) impaired fungal clearance more prominently in the lung than in the kidney 24 h after intravenous infection withC. albicans.Rapid and transient production of IL-23 was detected in the lung at 12 h, preceding IL-17A production and the influx of neutrophils, which reached a peak at 24 h after infection. IL-17A knockout (KO) mice showed reduced infiltration of neutrophils concurrently with impaired fungal clearance in the lung after infection. The major source of IL-17A was the γδ T cell population in the lung, and Cδ KO mice showed little IL-17A production and reduced neutrophil infiltration after infection. Early IL-23 production in a TLR2/MyD88-dependent manner and IL-23-triggered tyrosine kinase 2 (Tyk2) signaling were essential for IL-17A production by γδ T cells. Thus, our study demonstrated a novel role of naturally occurring IL-17A-producing γδ T cells in the first line of host defense againstC. albicansinfection.


2018 ◽  
Vol 19 (5) ◽  
pp. 464-474 ◽  
Author(s):  
Ayano C. Kohlgruber ◽  
Shani T. Gal-Oz ◽  
Nelson M. LaMarche ◽  
Moto Shimazaki ◽  
Danielle Duquette ◽  
...  

2019 ◽  
Vol 20 (3) ◽  
pp. 373-373
Author(s):  
Ayano C. Kohlgruber ◽  
Shani T. Gal-Oz ◽  
Nelson M. LaMarche ◽  
Moto Shimazaki ◽  
Danielle Duquette ◽  
...  

2004 ◽  
Vol 172 (12) ◽  
pp. 7629-7634 ◽  
Author(s):  
Kaori Uezu ◽  
Kazuyoshi Kawakami ◽  
Kazuya Miyagi ◽  
Yuki Kinjo ◽  
Takeshi Kinjo ◽  
...  

Immunity ◽  
2016 ◽  
Vol 45 (5) ◽  
pp. 999-1012 ◽  
Author(s):  
Noriyuki Fujikado ◽  
Alexander O. Mann ◽  
Kushagra Bansal ◽  
Kimberly R. Romito ◽  
Elise M.N. Ferre ◽  
...  

2013 ◽  
Vol 81 (10) ◽  
pp. 3923-3934 ◽  
Author(s):  
Ying Guo ◽  
Xun Sun ◽  
Kensuke Shibata ◽  
Hisakata Yamada ◽  
Hiromi Muta ◽  
...  

ABSTRACTInterleukin-17A (IL-17A)-producing γδ T cells are known to be activated followingMycobacterium bovisbacillus Calmette-Guérin (BCG) infection. Here, we show that CD30, a member of the tumor necrosis factor (TNF) receptor superfamily, is important for activation of IL-17A-producing γδ T cells after BCG infection. Vγ1−Vγ4−γδ T cells preferentially expressing Vγ6/Vδ1 genes were identified as the major source of IL-17A in the peritoneal cavity during the early stage of BCG infection. The number of IL-17A-producing Vγ1−Vγ4−γδ T cells bearing Vγ6 increased in peritoneal exudate cells (PEC) of wild-type (WT) mice but not in those of CD30 knockout (KO) mice in response to BCG infection. Consistently, CD30 ligand (CD30L) or CD30 expression, predominantly by Vγ1−Vγ4−γδ T cells, was rapidly upregulated after BCG infection. Inhibition of CD30L/CD30 signaling byin vivoadministration of a soluble CD30 and immunoglobulin fusion protein (CD30-Ig) severely impaired activation of IL-17A-producing Vγ1−Vγ4−γδ T cells in WT mice, while stimulating CD30L/CD30 signaling byin vivoadministration of agonistic anti-CD30 monoclonal antibody (MAb) restored IL-17A production by Vγ1−Vγ4−γδ T cells in CD30L KO mice after BCG infection. These results suggest that CD30 signaling plays an important role in the activation of IL-17A-producing Vγ1−Vγ4−γδ T cells bearing Vγ6 at an early stage of BCG infection.


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