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  • The American Association of Immunologists  (14)
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  • The American Association of Immunologists  (14)
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  • 1
    Online Resource
    Online Resource
    Neutrophils Promote Amphiregulin Production in Intestinal Epithelial Cells through TGF-β and Contribute to Intestinal Homeostasis
    The American Association of Immunologists ; 2018
    In:  The Journal of Immunology Vol. 201, No. 8 ( 2018-10-15), p. 2492-2501
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 201, No. 8 ( 2018-10-15), p. 2492-2501
    Abstract: Neutrophils are the first responders to sites of inflammation when the intestinal epithelial barrier is breached and the gut microbiota invade. Despite current efforts in understanding the role of neutrophils in intestinal homeostasis, the complex interactions between neutrophils and intestinal epithelial cells (IECs) is still not well characterized. In this study, we demonstrated that neutrophils enhanced production of amphiregulin (AREG), a member of the EGFR ligand family, by IECs, which promoted IEC barrier function and tissue repair. Depletion of neutrophils resulted in more severe colitis in mice because of decreased AREG production by IECs upon dextran sodium sulfate (DSS) insult. Administration of AREG restored epithelial barrier function and ameliorated colitis. Furthermore, neutrophil-derived TGF-β promoted AREG production by IECs. Mechanistically, TGF-β activated MEK1/2 signaling, and inhibition of MEK1/2 abrogated TGF-β–induced AREG production by IECs. Collectively, these findings reveal that neutrophils play an important role in the maintenance of IEC barrier function and homeostasis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1800003
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2018
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 2
    Online Resource
    Online Resource
    Tumor exosomes inhibit differentiation of bone marrow dendritic cells (49.14)
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 1_Supplement ( 2007-04-01), p. S85-S85
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 1_Supplement ( 2007-04-01), p. S85-S85
    Abstract: The production of exosomes by tumor cells has been implicated in tumor-associated immune suppression. Here we show that, in mice, exosomes produced by TS/A murine mammary tumor cells target CD11b+Gr-1+ myeloid precursors in the bone marrow in vivo and that this is associated with an accumulation of myeloid precursors in the spleen. Moreover, we demonstrate that TS/A exosomes block differentiation of murine myeloid precursor cells into dendritic cells in vitro. Addition of tumor exosomes at day 0 led to a complete block of differentiation into dendritic cells, whereas addition at later time points was less effective. Similarly, exosomes produced by human breast tumor cells inhibited differentiation of human monocytes in vitro. The levels of IL-6 and phosphorylated Stat3 were elevated 12 h after tumor exosome stimulation of murine myeloid precursors, and tumor exosomes were less effective in inhibiting differentiation of bone marrow cells isolated from IL-6 knockout mice. These data suggest that tumor exosome-mediated induction of IL-6 plays a role in blocking bone marrow dendritic cell differentiation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.Supp.49.14
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 3
    Online Resource
    Online Resource
    Commensal flagellated A4 bacteria inhibit intestinal Th2 responses through induction of innate cell TGFβ production (MUC9P.742)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 205.6-205.6
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 205.6-205.6
    Abstract: Interaction between host and microbiota maintains intestinal immune homeostasis. While commensal bacteria promotes Th1, Th17, and Tregs cells in lamina propria (LP) in the steady condition, it suppresses mucosal Th2 cells. Some specific commensal organisms have defined effects on mucosal immune function, e.g., SFB preferably promotes intestinal Th17 while certain Clostridium spp induce Tregs. However, it is still unclear whether there are specific commensal organisms down-regulating Th2 responses, and the mechanism involved. In this report, we showed that there were more LP Th2 cells in germ-free mice compared to the mice under SPF conditions. A4 bacteria, a commensal isolated from mouse cecum and produces immunodominant microbiota antigen, CBir1 flagellin, presented in intestinal lumen. In CBir1 TCR Tg mice, Th1, Th17 and Treg but not Th2 cells were present in the intestinal LP. When stimulated with CBir1 flagellin, naïve CBir1 Tg T cells differentiated into Th1, Th17 and Tregs but resisted Th2 differentiation. Aaddition of A4 bacteria, as well as pretreatment of APC with A4 bacteria, inhibited Th2 differentiation of OTII T cells stimulated with OVA and of wild-type T cells stimulated with anti-CD3 under Th2 polarizing conditions. A4 bacteria stimulated DC production of TGFβ, blockade of TGFβ abrogated A4 inhibition of Th2 cell development. Collectively, our data reveal that A4 bacteria inhibit intestinal Th2 responses through induction of innate cell production of TGFβ.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.205.6
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 4
    Online Resource
    Online Resource
    Tumor Exosomes Inhibit Differentiation of Bone Marrow Dendritic Cells
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 11 ( 2007-06-01), p. 6867-6875
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 11 ( 2007-06-01), p. 6867-6875
    Abstract: The production of exosomes by tumor cells has been implicated in tumor-associated immune suppression. In this study, we show that, in mice, exosomes produced by TS/A murine mammary tumor cells target CD11b+ myeloid precursors in the bone marrow (BM) in vivo, and that this is associated with an accumulation of myeloid precursors in the spleen. Moreover, we demonstrate that TS/A exosomes block the differentiation of murine myeloid precursor cells into dendritic cells (DC) in vitro. Addition of tumor exosomes at day 0 led to a significant block of differentiation into DC, whereas addition at later time points was less effective. Similarly, exosomes produced by human breast tumor cells inhibited the differentiation of human monocytes in vitro. The levels of IL-6 and phosphorylated Stat3 were elevated 12 h after the tumor exosome stimulation of murine myeloid precursors, and tumor exosomes were less effective in inhibiting differentiation of BM cells isolated from IL-6 knockout mice. Addition of a rIL-6 to the IL-6 knockout BM cell culture restored the tumor exosome-mediated inhibition of DC differentiation. These data suggest that tumor exosome-mediated induction of IL-6 plays a role in blocking BM DC differentiation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.11.6867
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 5
    Online Resource
    Online Resource
    Microbiota Downregulates Dendritic Cell Expression of miR-10a, Which Targets IL-12/IL-23p40
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 187, No. 11 ( 2011-12-01), p. 5879-5886
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 187, No. 11 ( 2011-12-01), p. 5879-5886
    Abstract: Commensal flora plays important roles in the regulation of the gene expression involved in many intestinal functions and the maintenance of immune homeostasis, as well as in the pathogenesis of inflammatory bowel diseases. The microRNAs (miRNAs), a class of small, noncoding RNAs, act as key regulators in many biological processes. The miRNAs are highly conserved among species and appear to play important roles in both innate and adaptive immunity, as they can control the differentiation of various immune cells, as well as their functions. However, it is still largely unknown how microbiota regulates miRNA expression, thereby contributing to intestinal homeostasis and pathogenesis of inflammatory bowel disease. In our current study, we found that microbiota negatively regulated intestinal miR-10a expression, because the intestines, as well as intestinal epithelial cells and dendritic cells of specific pathogen-free mice, expressed much lower levels of miR-10a compared with those in germ-free mice. Commensal bacteria downregulated dendritic cell miR-10a expression via TLR–TLR ligand interactions through a MyD88-dependent pathway. We identified IL-12/IL-23p40, a key molecule for innate immune responses to commensal bacteria, as a target of miR-10a. The ectopic expression of the miR-10a precursor inhibited, whereas the miR-10a inhibitor promoted, the expression of IL-12/IL-23p40 in dendritic cells. Mice with colitis expressing higher levels of IL-12/IL-23p40 exhibited lower levels of intestinal miR-10a compared with control mice. Collectively, our data demonstrated that microbiota negatively regulates host miR-10a expression, which may contribute to the maintenance of intestinal homeostasis by targeting IL-12/IL-23p40 expression.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1100535
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 6
    Online Resource
    Online Resource
    Microbiota Metabolite Short-Chain Fatty Acids Facilitate Mucosal Adjuvant Activity of Cholera Toxin through GPR43
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 203, No. 1 ( 2019-07-01), p. 282-292
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 203, No. 1 ( 2019-07-01), p. 282-292
    Abstract: The gut microbiota has been shown critical for mucosal adjuvant activity of cholera toxin (CT), a potent mucosal adjuvant. However, the mechanisms involved remain largely unknown. In this study, we report that depletion of gut bacteria significantly decreased mucosal and systemic Ab responses in mice orally immunized with OVA and CT. Feeding mice short-chain fatty acids (SCFAs) promoted Ab responses elicited by CT, and, more importantly, rescued Ab responses in antibiotic-treated mice. In addition, mice deficient in GPR43, a receptor for SCFAs, showed impaired adjuvant activity of CT. Administering CT did not promote SCFA production in the intestines; thus, SCFAs facilitated but did not directly mediate the adjuvant activity of CT. SCFAs promoted B cell Ab production by promoting dendritic cell production of BAFF and ALDH1a2, which induced B cell expression of IFN regulatory factor 4, Blimp1, and XBP1, the plasma B cell differentiation-related genes. Furthermore, when infected with Citrobacter rodentium, GPR43−/− mice exhibited decreased Ab responses and were more susceptible to infection, whereas the administration of SCFAs promoted intestinal Ab responses in wild-type mice. Our study thereby demonstrated a critical role of gut microbiota and their metabolite SCFAs in promoting mucosal adjuvant activity of CT through GPR43.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1801068
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 7
    Online Resource
    Online Resource
    CCR9 regulates colitis development by inhibiting regulatory T cell development (MUC8P.725)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 204.5-204.5
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 204.5-204.5
    Abstract: T cells reactive to microbiota regulate the pathogenesis of inflammatory bowel disease (IBD). As T cell trafficking to intestines is regulated through interactions between highly specific chemokine-chemokine receptors, great efforts have been made to develop intestinal specific immunosuppression based on blocking these key processes. CCR9, a gut-trophic chemokine receptor expressed by lymphocytes and dendritic cells, has been implicated in regulation of IBD through mediating recruitment of T cells to inflamed sites. However, the role of CCR9 in inducing and sustaining inflammation in the context of IBD is poorly understood. In the current study, we demonstrate that CCR9 inhibits Treg cell development, which contributes to its regulation of intestinal inflammation. While CCR9-/- mice are more resistant to disease compared to wild type (WT) mice upon DSS insults, CCR9 deficiency does not affect effector T cell induction of colitis in a microbiota antigen specific T cell-mediated model. Interestingly, CCR9-/- mice demonstrate a high level of Foxp3+ Tregs, and ligation of CCR9 by its ligand CCL25 inhibited Treg cell differentiation in vitro. Furthermore, partial depletion of Tregs in CCR9-/- mice increased susceptibility to DSS insults to a level similar to WT mice. Collectively, our data indicates that CCR9 signaling inhibits Treg cell development, which contributes to its regulation of colitis development, in addition to acting as a gut-homing molecule.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.204.5
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 8
    Online Resource
    Online Resource
    Correction: RORγt Represses IL-10 Production in Th17 Cells To Maintain Their Pathogenicity in Inducing Intestinal Inflammation
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 206, No. 11 ( 2021-06-01), p. 2764-2765
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 11 ( 2021-06-01), p. 2764-2765
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100271
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 9
    Online Resource
    Online Resource
    TGFβ converts Th1 cell into Th17 cells through stimulation of Runx1 expression under inflammatory conditions in intestines (MUC2P.819)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 68.3-68.3
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 68.3-68.3
    Abstract: Although accumulating evidence demonstrates that differentiated CD4 cells preserve plasticity to alter phenotypes under various conditions, it is still unclear how stable Th1 cells are and whether Th1 cells can convert into Th17 cells. The high stability of Th1 is supported by some epigenetic studies and numerous reports of Treg and Th17 cells conversion into Th1 cells but not vice versa. However, recent reports of Th1 cell conversion to Treg, Th2 and Tfh cells argue the absolute stability of Th1 lineage. By using IFNγThy1.1 CBir1 TCR transgenic reporter mice, whose TCR is specific for an immunodominant microbiota antigen, we investigate the stability of Th1 cells under intestinal inflammatory conditions. Transfer of purified CBir1 specific IFNγ+Th1 cells induces colitis in RAG-/- mice and IFNγ+Th1 cells convert into IL-17+ Th17 but not Foxp3+ Treg cells in the inflamed intestines. TGFβ, IL-6 and IL-2, but not hypoxia factors, differentially regulate Th1 to Th17 conversion. TGFβ induction of transcriptional factors, Runx1 and RORγt, is crucial for the conversion, in that silencing Runx1 by siRNA inhibits Th1 conversion into Th17 cells. Furthermore, using ChIP assay, we show that TGFβ enhances histone acetylation but inhibits trimethylation of Runx1 and RORγt binding sites on il-17 or rorc gene in Th1 cells. In conclusion, our data demonstrate that Th1 cells convert into Th17 cells under inflammatory conditions in intestines, which is mediated by TGFβ-induction of Runx1.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.68.3
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2014
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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  • 10
    Online Resource
    Online Resource
    MicroRNA-10a Negatively Regulates CD4+ T Cell IL-10 Production through Suppression of Blimp1
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 207, No. 3 ( 2021-08-01), p. 985-995
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 207, No. 3 ( 2021-08-01), p. 985-995
    Abstract: An uncontrolled CD4+ T cell response is a critical hallmark of autoimmune diseases. IL-10, which can be produced by both effector and regulatory CD4+ T cells, plays an essential role in the inhibition of autoimmunity. MicroRNAs are key molecules involved in regulating immune responses. However, how miR-10a regulates CD4+ T cell function in the pathogenesis of intestinal immune responses is not fully understood. In this study, we show that the mice with deficient miR-10a in CD4+ T cells were more resistant to intestinal inflammation upon inflammatory insult. miR-10a–deficient CD4+CD45Rbhi T cells were less colitogenic in Rag−/− mice, in which CD4+ T cell production of IL-10 was increased. miR-10a–deficient CD4+ T cells expressed a higher expression of IL-10 in vitro. Blocking the IL-10/IL-10R pathway in vivo aggravated colitis induced by miR-10a–deficient CD4+CD45Rbhi T cells. Mechanically, miR-10a suppressed CD4+ T cell production of IL-10 through targeting Prdm1, which encodes Blimp1. We further show that that CD4+ T cells lacking Blimp1 produced lower levels of IL-10 and induced more severe colitis in Rag−/− mice. These data thus establish the role of miR-10a in the inhibition of IL-10 production in CD4+ T cells to regulate intestinal homeostasis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100017
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
    detail.hit.zdb_id: 3056-9
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