Escherichia coli infection induces only fetal thymus-derived γ δ T cells at the infected site

γδ T lymphocytes have been shown to regulate immune responses in diverse experimental systems. Because distinct γδ T cell subsets, as defined by the usage of certain TCR V genes, preferentially respond in various diseases and disease models, we have hypothesized that the various γδ T cell subsets carry out different functions. To test this, we compared one particular γδ T cell subset, the Vγ1+ subset, which represents a major γδ T cell type in the lymphoid organs and blood of mice, to other subsets and to γδ T cells as a whole. Using Listeria monocytogenes infection as an infectious disease model, we found that bacterial containment improves in mice depleted of Vγ1+ γδ T cells, albeit mice lacking all γδ T cells are instead impaired in their ability to control Listeria expansion. Our findings indicate that Vγ1+ γδ T cells reduce the ability of the innate immune system to destroy Listeria, even though other γδ T cells as a whole promote clearance of this pathogen.

mentioning

confidence: 65%

Depletion of a γδ T Cell Subset Can Increase Host Resistance to a Bacterial Infection

O’Brien

Yin

Huber

et al. 2000

“…We and others (33)(34)(35) previously reported that i.p. infection of mice with E. coli induced a marked increase in ␥␦ T cells in the peritoneal cavity (33,34,36) and that the ␥␦ T cells had a protective role against the infection (37).…”

mentioning

confidence: 78%

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

Mokuno

Matsuguchi²,

Takano

et al. 2000

133

125

We recently reported that the number of γδ T cells was increased after infection with Escherichia coli in C3H/HeN mice. We here showed that an i.p. injection with native lipid A derived from E. coli induced an increase of γδ T cells in the peritoneal cavity of LPS-responsive C3H/HeN mice and, albeit to a lesser degree, also in LPS-hyporesponsive C3H/HeJ mice. The purified γδ T cells from C3H/HeN and C3H/HeJ mice expressed a canonical TCR repertoire encoded by Vγ6-Jγ1/Vδ1-Dδ2-Jδ2 gene segments and proliferated in response to the native lipid A derived from E. coli in a TCR-independent manner. The lipid A-reactive γδ T cells bearing canonical Vγ6/Vδ1 expressed Toll-like receptor (TLR) 2 mRNA, while TLR4 mRNA was undetectable. Treatment with a TLR2 anti-sense oligonucleotide resulted in hyporesponsiveness of the γδ T cells to the native lipid A. TLR2-deficient mice showed an impaired increase of the γδ T cells following injection of native lipid A. These results suggest that TLR2 is involved in the activation of canonical Vγ6/Vδ1 T cells by native E. coli lipid A.

“…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%

“…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

436

410

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.