scholarly journals Extensive and Preferential Fas/Fas Ligand-Dependent Death of γδ T Cells Following Infection with Listeria monocytogenes

2002 ◽  
Vol 56 (3) ◽  
pp. 233-247 ◽  
Author(s):  
A. MUKASA ◽  
M. LAHN ◽  
S. FLEMING ◽  
B. FREIBERG ◽  
E. PFLUM ◽  
...  
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
Fas Ligand ◽  
Γδ T Cells

scholarly journals IL-17A–producing resident memory γδ T cells orchestrate the innate immune response to secondary oral Listeria monocytogenes infection

2016 ◽  
Vol 113 (30) ◽  
pp. 8502-8507 ◽  
Author(s):  
Pablo A. Romagnoli ◽  
Brian S. Sheridan ◽  
Quynh-Mai Pham ◽  
Leo Lefrançois ◽  
Kamal M. Khanna
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
Chemokine Receptor ◽  
Myeloid Cells ◽  
Γδ T Cells ◽  
Oral Infection ◽  
Mesenteric Lymph Nodes ◽  
Intestinal Pathogens ◽  
Replication Foci ◽  
Static Pattern

Memory γδ T cells are important for the clearance of Listeria monocytogenes infection in the intestinal mucosa. However, the mechanisms by which memory γδ T cells provide protection against secondary oral infection are poorly understood. Here we used a recombinant strain of L. monocytogenes that efficiently invades the intestinal epithelium to show that Vγ4+ memory γδ T cells represent a resident memory (Trm) population in the mesenteric lymph nodes (MLNs). The γδ Trm exhibited a remarkably static pattern of migration that radically changed following secondary oral L. monocytogenes infection. The γδ Trms produced IL-17A early after rechallenge and formed organized clusters with myeloid cells surrounding L. monocytogenes replication foci only after a secondary oral infection. Antibody blocking studies showed that in addition to IL-17A, the chemokine receptor C-X-C chemokine receptor 3 (CXCR3) is also important to enable the local redistribution of γδ Trm cells and myeloid cells specifically near the sites of L. monocytogenes replication within the MLN to restrict bacterial growth and spread. Our findings support a role for γδ Trms in orchestrating protective immune responses against intestinal pathogens.

scholarly journals Human γδ T Cells Augment Antigen Presentation in Listeria Monocytogenes Infection

2016 ◽  
Vol 22 (1) ◽  
pp. 737-746 ◽  
Author(s):  
Yuli Zhu ◽  
Huaishan Wang ◽  
Yi Xu ◽  
Yu Hu ◽  
Hui Chen ◽  
...  
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
Antigen Presentation ◽  
Γδ T Cells ◽  
Listeria Monocytogenes Infection

scholarly journals High Expression of Fas Ligand by Synovial Fluid-Derived γδ T Cells in Lyme Arthritis

2003 ◽  
Vol 170 (5) ◽  
pp. 2702-2710 ◽  
Author(s):  
Karen Roessner ◽  
Julie Wolfe ◽  
Cuixia Shi ◽  
Leonard H. Sigal ◽  
Sally Huber ◽  
...  
Keyword(s):  
T Cells ◽  
Synovial Fluid ◽  
Fas Ligand ◽  
Γδ T Cells ◽  
Lyme Arthritis ◽  
High Expression

scholarly journals Lyme Arthritis Synovial γδ T Cells Instruct Dendritic Cells via Fas Ligand

2005 ◽  
Vol 175 (9) ◽  
pp. 5656-5665 ◽  
Author(s):  
Cheryl Collins ◽  
Julie Wolfe ◽  
Karen Roessner ◽  
Cuixia Shi ◽  
Leonard H. Sigal ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Fas Ligand ◽  
Γδ T Cells ◽  
Lyme Arthritis

scholarly journals Fas-Fas Ligand Interactions Are Essential for the Binding to and Killing of Activated Macrophages by γδ T Cells

2004 ◽  
Vol 173 (6) ◽  
pp. 3660-3667 ◽  
Author(s):  
Jane E. Dalton ◽  
Gareth Howell ◽  
Jayne Pearson ◽  
Phillip Scott ◽  
Simon R. Carding
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
Γδ T Cells ◽  
Activated Macrophages ◽  
Ligand Interactions

scholarly journals Disruption of the Cellular Inflammatory Response to Listeria monocytogenes Infection in Mice with Disruptions in Targeted Genes

1998 ◽  
Vol 66 (5) ◽  
pp. 2284-2289 ◽  
Author(s):  
J. DiTirro ◽  
E. R. Rhoades ◽  
A. D. Roberts ◽  
J. M. Burke ◽  
A. Mukasa ◽  
...  
Keyword(s):  
T Cells ◽  
Listeria Monocytogenes ◽  
T Cell ◽  
Knockout Mice ◽  
Γδ T Cells ◽  
Mononuclear Phagocytes ◽  
Γδ T Cell ◽  
Cellular Inflammatory Response ◽  
Successful Resolution ◽  
Knockout Animals

ABSTRACT The results of this study to dissect the nature of the acquired immune response to infection with Listeria monocytogenes in mice with targetted gene disruptions show that successful resolution of disease requires the essential presence of αβ T cells and the capacity to elaborate gamma interferon. In the absence of either of these entities, mice experience increasingly severe hepatitis and tissue necrosis and die within a few days. The data from this study support the hypothesis that the protective process is the efficient replacement of neutrophils in lesions by longer-lived mononuclear phagocytes; αβ-T-cell-knockout mice died from progressive infection before neutrophil replacement could occur, whereas in γδ-T-cell-knockout mice this replacement process in the liver has previously been shown to be much slower. In the present study we attribute this delay to reduced production of the macrophage-attracting chemokine MCP-1 in the γδ-T-cell-knockout animals. These data further support the hypothesis that γδ T cells are important in controlling the inflammatory process rather than being essential to the expression of protection.

scholarly journals γδ T Cells Promote a Th1 Response during Coxsackievirus B3 Infection In Vivo: Role of Fas and Fas Ligand

2002 ◽  
Vol 76 (13) ◽  
pp. 6487-6494 ◽  
Author(s):  
Sally Huber ◽  
Cuixia Shi ◽  
Ralph C. Budd
Keyword(s):  
T Cells ◽  
Fas Ligand ◽  
High Surface ◽  
Γδ T Cells ◽  
Coxsackievirus B3 ◽  
Interleukin 4 ◽  
Cell Phenotype ◽  
Th1 Cell ◽  
Cvb3 Infection

ABSTRACT Fas/Fas ligand (FasL) interactions regulate disease outcome in coxsackievirus B3 (CVB3)-induced myocarditis. MRL+/+ mice infected with CVB3 develop severe myocarditis, a dominant CD4+ Th1 (gamma interferon [IFN-γ+]) response to the virus, and a predominance of γδ T cells in the myocardial infiltrates. MRL lpr/lpr and MRL gld/gld mice, which lack normal expression of Fas and express a mutated FasL, respectively, have minimal myocarditis and show a dominant CD4+ Th2 (interleukin-4 [IL-4+]) phenotype to CVB3. Spleen cells from virus-infected wild-type, lpr, and gld animals proliferate equally to virus in vitro. Adoptive transfer of γδ T cells from hearts of CVB3-infected MRL+/+ mice (FasL+) into infected MRL gld/gld recipients (FasL−/Fas+) restores both disease susceptibility and Th1 cell phenotype. However, transfer of these cells into MRL lpr/lpr recipients (FasL+/Fas−) did not promote myocarditis and the viral response remained Th2 biased. This paralleled the expression of very high surface levels of FasL by myocardial γδ T cells, as well as their propensity to selectively lyse Th2 virus-specific CD4+ T cells. These results demonstrate that Fas/FasL interactions conferred by γδ Τ cells on lymphocyte subpopulations may regulate the cytokine response to CVB3 infection and pathogenicity.

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