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  • Oxford University Press (OUP)  (9)
  • Yang, Ping-Chang  (9)
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  • Oxford University Press (OUP)  (9)
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  • 1
    Online Resource
    Online Resource
    Intestinal epithelial cell-derived integrin αβ6 plays an important role in the induction of regulatory T cells and inhibits an antigen-specific Th2 response
    Oxford University Press (OUP) ; 2011
    In:  Journal of Leukocyte Biology Vol. 90, No. 4 ( 2011-07-01), p. 751-759
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 90, No. 4 ( 2011-07-01), p. 751-759
    Abstract: Toleroge nic DCs and Tregs are believed to play a critical role in oral tolerance. However, the mechanisms of the generation of tolerogenic DCs and activation of Tregs in the gut remain poorly understood. This study aims to dissect the molecular mechanisms by which IECs and protein antigen induce functional tolerogenic DCs and Tregs. Expression of αvβ6 by gut epithelial cell-derived exosomes, its coupling with food antigen, and their relationship with the development of functional tolerogenic DCs and Tregs were examined by using in vitro and in vivo approaches. The results show that IECs up-regulated the integrin αvβ6 upon uptake of antigens. The epithelial cell-derived exosomes entrapped and transported αvβ6 and antigens to the extracellular environment. The uptake of antigens alone induced DCs to produce LTGFβ, whereas exosomes carrying αvβ6/antigen resulted in the production of abundant, active TGF-β in DCs that conferred to DCs the tolerogenic properties. Furthermore, αvβ6/OVA-carrying, exosome-primed DCs were found to promote the production of active TGF-β in Tregs. Thus, in vivo administration of αvβ6/OVA-laden exosomes induced the generation of Tregs and suppressed skewed Th2 responses toward food antigen in the intestine. Our study provides important molecular insights into the molecular mechanisms of Treg development by demonstrating an important role of IEC-derived exosomes carrying αvβ6 and food antigen in the induction of tolerogenic DCs and antigen-specific Tregs.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.1210696
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Enolase-specific cross antibodies induce neutrophilic inflammation in the intestine
    Oxford University Press (OUP) ; 2021
    In:  Journal of Leukocyte Biology Vol. 109, No. 3 ( 2021-03-01), p. 633-644
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 109, No. 3 ( 2021-03-01), p. 633-644
    Abstract: The pathogenesis of ulcerative colitis (UC) is to be further investigated. House dust mites (HDM) are highly associated with the pathogenesis of immune inflammation in the body. This study aims to investigate the role of enolase (one of the HDM-derived proteins)-specific cross Abs in the induction of UC-like inflammation. The enolase specific IgG (EsIgG) was identified in UC patients by mass spectrometry. Mice were treated with EsIgG to induce inflammation in the colon mucosa. EsIgG was detected in the serum and the colon tissues of UC patients, which was positively correlated with the polymorphonuclear neutrophil (PMN) counts in the blood and colon tissues of UC patients. EsIgG formed immune complexes with the constitutive enolase in the UC colon epithelium that activated complement, induced epithelial cell apoptosis, compromised epithelial barrier functions, and resulted in UC-like inflammation in the mouse colon. In summary, UC patients have high serum levels of Abs against HDM-derived enolase and intestinal epithelial cell-derived enolase. These Abs attack the colonic epithelium to induce UC-like inflammation.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1002/JLB.3A0620-128R
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Characterization of allergic inflammation in chronic uterine cervicitis
    Oxford University Press (OUP) ; 2022
    In:  Clinical and Experimental Immunology Vol. 207, No. 1 ( 2022-01-28), p. 44-52
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 207, No. 1 ( 2022-01-28), p. 44-52
    Abstract: Female genital tract chronic inflammation is common in clinics; the pathogenesis is not fully understood yet. House dust mite (HDM) involves the pathogenesis of many chronic diseases in human. This study aims to identify HDM-specific allergic response in the cervix of patients with cervical inflammation. Patients (n = 80) with chronic cervicitis (CC) and non-CC control (NC) subjects (n = 80) were recruited into this study. Vaginal lavage fluids (VLF) were collected from CC patients and NC subjects. Cellular components and fluid part of VLF were separated by centrifugation, and analyzed by flow cytometry and enzyme-linked immunosorbent assay. We found that a portion (52 out of 80) of CC patients responded to HDM, manifesting positive skin prick test, and HDM-specific IgE and IgG was detected in the VLF (designated CCp patients). VLF of CCp patients showed a Th2-dominant profile. HDM-specific Th2 cells were detected in VLF in CCp patients. Exposure to HDM in the culture induced proinflammatory cytokine release from CCp VLF CD4+ T cells. Exposure to CCp VLF CD4+ T cell-conditioned medium induced de novo Th2 response. Direct exposure to HDM induced allergic response in the cervix of CCp patients. In summary, a portion of CC patients respond to HDM challenge in the cervix. Exposure to HDM induces an allergy-like response in the cervix of CCp patients.
    Type of Medium: Online Resource
    ISSN: 0009-9104 , 1365-2249
    URL: Article
    DOI: 10.1093/cei/uxab026
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2020024-9
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  • 4
    Online Resource
    Online Resource
    Vitamin D receptor restricts T helper 2-biased inflammation in the heart
    Oxford University Press (OUP) ; 2018
    In:  Cardiovascular Research Vol. 114, No. 6 ( 2018-05-01), p. 870-879
    Details
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 114, No. 6 ( 2018-05-01), p. 870-879
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    URL: Article
    DOI: 10.1093/cvr/cvy034
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 1499917-1
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  • 5
    Online Resource
    Online Resource
    Frontline Science: TLR3 activation inhibits food allergy in mice by inducing IFN-γ+ Foxp3+ regulatory T cells
    Oxford University Press (OUP) ; 2019
    In:  Journal of Leukocyte Biology Vol. 106, No. 6 ( 2019-11-28), p. 1201-1209
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 106, No. 6 ( 2019-11-28), p. 1201-1209
    Abstract: The pathologic feature of food allergy (FA) is the aberrant Th2-biased immune response in the intestine. Regulatory T cells (Tregs) play an important role in the suppression of aberrant immune response. The activities of the TLRs regulate multiple cell functions. This study aims to investigate the role of TLR3 activation in the regulation of Th2-biased immune response in the intestine by the generation of inducible Tregs (iTregs). In this study, polyinosinic polycytidylic acid (polyI:C) was used as an activator of TLR3. An FA mouse model was developed to establish the Th2-biased inflammation in the intestine. The effects of TLR3 activation on the generation of iTreg were tested in the culture and in mice. We observed that exposure to polyI:C induced IFN-γ+ Foxp3+ iTregs in mouse intestine and in the culture. The IFN-γ+ Foxp3+ iTregs showed immune suppressive functions. Exposure to polyI:C increased T-bet levels in CD4+ T cells. The T-bet formed a complex with GATA3 to dissociate Foxp3 from GATA3/Foxp3 complex in CD4+ T cells. The Foxp3 thus gained the opportunity to move to TGF-β promoter to generate iTregs. Administration with polyI:C prevented the development of FA and inhibited existing FA. In conclusion, activation of TLR3 induces IFN-γ+ Foxp3+ Tregs, which can prevent FA development and inhibit existing FA in mice.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1002/JLB.3HI0918-348RR
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    The increased expression of IL-23 in inflammatory bowel disease promotes intraepithelial and lamina propria lymphocyte inflammatory responses and cytotoxicity
    Oxford University Press (OUP) ; 2011
    In:  Journal of Leukocyte Biology Vol. 89, No. 4 ( 2011-01-07), p. 597-606
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 89, No. 4 ( 2011-01-07), p. 597-606
    Abstract: This study analyzed IL-23p19 expression in inflamed mucosa of IBD and the role in the induction of IEL and NK cell activation as well as Th17 cell differentiation. Expression of IL-23p19 was performed by immunohistochemistry and quantitative real-time PCR. Expression of IL-23R was assessed by flow cytometry. Cytolytic activities of IEL and NK cells by IL-23 were determined by a standard 51Cr-release assay. Cytokine levels were analyzed by ELISA and quantitative real-time PCR. Expression of IL-23p19 was increased significantly in inflamed mucosa of CD compared with that in UC and healthy controls. Double-staining confirmed that IL-23p19+ cells were mainly CD68+ macrophages/DCs. IL-23R+ cells were increased significantly in PB- and LP-CD4+ and -CD8+ T and NK cells. IL-23 markedly promoted IBD IEL and NK cell activation and cytotoxicity and triggered IBD PB- and LP-T cells to secrete significantly higher levels of IFN-γ, TNF, IL-2, and IL-17A compared with controls. Importantly, IL-23 promoted IBD PB- or LP-CD4+ T cells to differentiate into Th17 cells, characterized by increased expression of IL-17A and RORC. Anti-TNF treatment could markedly reduce IL-23 expression and Th17 cell infiltration in inflamed mucosa of CD patients. These data indicate that IL-23 is highly expressed in inflamed mucosa of IBD and plays an important role in the induction of IEL, NK, and T cell activation, proinflammatory cytokine secretion, and Th17 cell differentiation. Targeted therapy directed against IL-23p19 may have a therapeutic role in treatment of IBD.
    Type of Medium: Online Resource
    ISSN: 0741-5400 , 1938-3673
    URL: Article
    DOI: 10.1189/jlb.0810456
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2026833-6
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Interleukin-5 induces apoptotic defects in CD4+ T cells of patients with allergic rhinitis
    Oxford University Press (OUP) ; 2019
    In:  Journal of Leukocyte Biology Vol. 105, No. 4 ( 2019-03-22), p. 719-727
    Details
    In: Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 105, No. 4 ( 2019-03-22), p. 719-727
    Abstract: T helper (Th)2 polarization plays an important role in the pathogenesis of allergic diseases; the underlying mechanism remains to be further investigated. B cell lymphoma protein-2 like protein-12 (Bcl2L12) has the anti-apoptotic function. This study aims to elucidate the contribution of Bcl2L12 to Th2 polarization in patients with allergic rhinitis (AR). In this study, human CD4+ T cells were isolated from blood samples collected from AR patients and healthy control (HC) subjects. The immune response profiles of CD4+ T cells were analyzed by immunologic approaches. The results showed that AR CD4+ T cells (CD4+ T cells collected from AR patients) showed defects of apoptosis. The expression of FasL in AR CD4+ T cells was lower than that of HC CD4+ T cells. Serum IL-5 levels were negatively correlated with the expression of FasL in AR CD4+ T cells. Exposure of CD4+ T cells to IL-5 in the culture suppressed the expression of FasL and increased the expression of Bcl2L12. IL-5 increased the levels of Bcl2L12 in CD4+ T cells, the latter bound to the FasL promoter to prevent FasL gene transcription. Inhibition of Bcl2L12 restored the apoptosis machinery in AR CD4+ T cells. In conclusion, overexpression of Bcl2L12 in CD4+ T cells compromises the apoptosis machinery; the latter can be restored by inhibition of Bcl2L12. BcL2L12 in CD4+ T cells may be a novel target for the treatment of AR and other allergic disorders.
    Type of Medium: Online Resource
    ISSN: 1938-3673 , 0741-5400
    URL: Article
    DOI: 10.1002/JLB.3A0718-287RR
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 2026833-6
    SSG: 12
    Location Call Number Limitation Availability
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    Online Resource
  • 8
    Online Resource
    Online Resource
    Correlation between cyclical epithelial barrier dysfunction and bacterial translocation in the relapses of intestinal inflammation
    Oxford University Press (OUP) ; 2006
    In:  Inflammatory Bowel Diseases Vol. 12, No. 9 ( 2006-09), p. 843-852
    Details
    In: Inflammatory Bowel Diseases, Oxford University Press (OUP), Vol. 12, No. 9 ( 2006-09), p. 843-852
    Type of Medium: Online Resource
    ISSN: 1078-0998
    URL: Article
    DOI: 10.1097/01.mib.0000231571.88806.62
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2006
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  • 9
    Online Resource
    Online Resource
    T cell activator-carrying extracellular vesicles induce antigen-specific regulatory T cells
    Oxford University Press (OUP) ; 2021
    In:  Clinical and Experimental Immunology Vol. 206, No. 2 ( 2021-10-12), p. 129-140
    Details
    In: Clinical and Experimental Immunology, Oxford University Press (OUP), Vol. 206, No. 2 ( 2021-10-12), p. 129-140
    Abstract: The mechanism of antigen-specific regulatory T cell (Treg) induction is not yet fully understood. Curcumin has an immune regulatory function. This study aims to induce antigen-specific Tregs by employing extracellular vesicles (EVs) that carry two types of T cell activators. Two types of T cell activators, ovalbumin (OVA)/major histocompatibility complex-II (MHC-II) and tetramethylcurcumin (FLLL31) (a curcumin analog) were carried by dendritic cell-derived extracellular vesicles, designated OFexo. A murine model of allergic rhinitis (AR) was developed with OVA as the specific antigen. AR mice were treated with a nasal instillation containing OFexo. We observed that OFexo recognized antigen-specific T cell receptors (TCR) on CD4+ T cells and enhanced Il10 gene transcription in CD4+ T cells. Administration of the OFexo-containing nasal instillation induced antigen-specific type 1 Tregs (Tr1 cells) in the mouse airway tissues. OFexo-induced Tr1 cells showed immune suppressive functions on CD4+ T cell proliferation. Administration of OFexo efficiently alleviated experimental AR in mice. In conclusion, OFexo can induce antigen-specific Tr1 cells that can efficiently alleviate experimental AR. The results suggest that OFexo has the translational potential to be employed for the treatment of AR or other allergic disorders.
    Type of Medium: Online Resource
    ISSN: 0009-9104 , 1365-2249
    URL: Article
    DOI: 10.1111/cei.13655
    RVK:
    XA 36770
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2020024-9
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