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  1. Article ; Online: TGF-β

    Zhijuan Qiu / Timothy H. Chu / Brian S. Sheridan

    Cells, Vol 10, Iss 989, p

    Many Paths to CD103 + CD8 T Cell Residency

    2021  Volume 989

    Abstract: CD8 tissue-resident memory T (T RM ) cells primarily reside in nonlymphoid tissues without recirculating and provide front-line protective immunity against infections and cancers. CD8 T RM cells can be generally divided into CD69 + CD103 − T RM cells ( ... ...

    Abstract CD8 tissue-resident memory T (T RM ) cells primarily reside in nonlymphoid tissues without recirculating and provide front-line protective immunity against infections and cancers. CD8 T RM cells can be generally divided into CD69 + CD103 − T RM cells (referred to as CD103 − T RM cells) and CD69 + CD103 + T RM cells (referred to as CD103 + T RM cells). TGF-β plays a critical role in the development and maintenance of CD103 + CD8 T RM cells. In this review, we summarize the current understanding of tissue-specific activation of TGF-β mediated by integrins and how it contributes to CD103 + CD8 T RM cell development and maintenance. Furthermore, we discuss the underlying mechanisms utilized by TGF-β to regulate the development and maintenance of CD103 + CD8 T RM cells. Overall, this review highlights the importance of TGF-β in regulating this unique subset of memory CD8 T cells that may shed light on improving vaccine design to target this population.
    Keywords CD8 tissue-resident memory T cells ; TGF-β ; CD103 ; integrin ; short-lived effector T cells ; memory precursor effector T cells ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: KLF5 protects the intestinal epithelium against Th17 immune response in a murine colitis model

    Jason Shieh / Timothy H. Chu / Yang Liu / Julie Kim / Ainara Ruiz de Sabando / Soma Kobayashi / Sui Y. Zee / Brian S. Sheridan / Agnieszka B. Bialkowska / Vincent W. Yang

    JCI Insight, Vol 7, Iss

    2022  Volume 7

    Abstract: Inflammatory bowel disease (IBD) is a chronic illness characterized by dysregulated immune cascades in the intestines, in which the Th17 immune response plays an important role. We demonstrated that mice with intestinal epithelium–specific deletion of ... ...

    Abstract Inflammatory bowel disease (IBD) is a chronic illness characterized by dysregulated immune cascades in the intestines, in which the Th17 immune response plays an important role. We demonstrated that mice with intestinal epithelium–specific deletion of Krüppel-like factor 5 (Klf5) developed Th17-dependent colonic inflammation. In the absence of KLF5, there was aberrant cellular localization of phosphorylated STAT3, an essential mediator of the Th17-associated cytokine, IL-22, which is required for epithelial tissue regeneration. In contrast, mitigation of IL-17A with anti–IL-17A neutralizing antibody attenuated colitis in Klf5-deficient mice. There was also a considerable shift in the colonic microbiota of Klf5-deficient mice that phenocopied human IBD. Notably, the inflammatory response due to Klf5 deletion was alleviated by antibiotic treatment, implicating the role of microbiota in pathogenesis. Finally, human colitic tissues had reduced KLF5 levels when compared with healthy tissues. Together, these findings demonstrated the importance of KLF5 in protecting the intestinal epithelium against Th17-mediated immune and inflammatory responses. The mice described herein may serve as a potential model for human IBD.
    Keywords Gastroenterology ; Inflammation ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Correction

    Timothy H. Chu / Camille Khairallah / Jason Shieh / Rhea Cho / Zhijuan Qiu / Yue Zhang / Onur Eskiocak / David G. Thanassi / Mark H. Kaplan / Semir Beyaz / Vincent W. Yang / James B. Bliska / Brian S. Sheridan

    PLoS Pathogens, Vol 18, Iss

    γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans

    2022  Volume 5

    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2022-05-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans.

    Timothy H Chu / Camille Khairallah / Jason Shieh / Rhea Cho / Zhijuan Qiu / Yue Zhang / Onur Eskiocak / David G Thanassi / Mark H Kaplan / Semir Beyaz / Vincent W Yang / James B Bliska / Brian S Sheridan

    PLoS Pathogens, Vol 17, Iss 12, p e

    2021  Volume 1010103

    Abstract: Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether ...

    Abstract Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether Y. pseudotuberculosis subverts these cells in mice and humans. Tracking Yop translocation revealed that the preferential delivery of Yop effectors directly into murine Vγ4 and human Vδ2+ T cells inhibited anti-microbial IFNγ production. Subversion was mediated by the adhesin YadA, injectisome component YopB, and translocated YopJ effector. A broad anti-pathogen gene signature and STAT4 phosphorylation levels were inhibited by translocated YopJ. Thus, Y. pseudotuberculosis attachment and translocation of YopJ directly into adaptive γδ T cells is a major mechanism of immune subversion in mice and humans. This study uncovered a conserved Y. pseudotuberculosis pathway that subverts adaptive γδ T cell function to promote pathogenicity.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans

    Timothy H. Chu / Camille Khairallah / Jason Shieh / Rhea Cho / Zhijuan Qiu / Yue Zhang / Onur Eskiocak / David G. Thanassi / Mark H. Kaplan / Semir Beyaz / Vincent W. Yang / James B. Bliska / Brian S. Sheridan

    PLoS Pathogens, Vol 17, Iss

    2021  Volume 12

    Abstract: Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether ...

    Abstract Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether Y. pseudotuberculosis subverts these cells in mice and humans. Tracking Yop translocation revealed that the preferential delivery of Yop effectors directly into murine Vγ4 and human Vδ2+ T cells inhibited anti-microbial IFNγ production. Subversion was mediated by the adhesin YadA, injectisome component YopB, and translocated YopJ effector. A broad anti-pathogen gene signature and STAT4 phosphorylation levels were inhibited by translocated YopJ. Thus, Y. pseudotuberculosis attachment and translocation of YopJ directly into adaptive γδ T cells is a major mechanism of immune subversion in mice and humans. This study uncovered a conserved Y. pseudotuberculosis pathway that subverts adaptive γδ T cell function to promote pathogenicity. Author summary Unconventional γδ T cells are a dynamic immune population important for mucosal protection of the intestine against invading pathogens. We determined that the foodborne pathogen Y. pseudotuberculosis preferentially targets an adaptive subset of these cells to subvert immune function. We found that direct injection of Yersinia outer proteins (Yop) into adaptive γδ T cells inhibited their anti-pathogen functions. We screened all Yop effectors and identified YopJ as the sole effector to inhibit adaptive γδ T cell production of IFNγ. We determined that adaptive γδ T cell subversion occurred by limiting activation of the transcription factor STAT4. When we infected mice with Y. pseudotuberculosis expressing an inactive YopJ, this enhanced the adaptive γδ T cell response and led to greater cytokine production from this subset of cells to aid mouse recovery. This mechanism of immune evasion appears conserved in humans as direct injection of Y. pseudotuberculosis YopJ into human γδ T cells inhibited cytokine production. This ...
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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