We are analyzing https://link.springer.com/protocol/10.1007/978-1-4939-2966-5_10.

Title:
In Vitro Th Differentiation Protocol | SpringerLink
Description:
CD4+ T cells play central roles in adaptive immunity, driving appropriate immune responses to invading pathogens of diverse types. Four major CD4+ T cell subsets, Th1, Th2, Th17, and Treg cells are differentiated from naïve CD4+ T cells upon ligation of their T...
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Keywords {🔍}

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Topics {✒️}

month download article/chapter tgf-beta-mediated regulation tgf-β signaling play central roles exclusively expressing ifn-γ device instant download privacy choices/manage cookies thymus-derived treg cells editor information editors tgf-β takashi sekiya fatal inflammatory disorders play important roles kinase-mediated interaction protocol sekiya european economic area mediate host defense mangan pr chronic mucocutaneous candidiasis harrington le journal finder publish conditions privacy policy pathogenic effector th17 reciprocal developmental pathways keio university school cd4-single positive accepting optional cookies excess activation results excess th2 activity author correspondence protocol cite interleukin 17-producing effector treg cells due helper cell fate pathogenic th17 cells helper cell differentiation protocol usd 49 main content log differentiation protocol signaling pathways interleukin-1 signaling social media hogquist ka critical cytokine permissions reprints interleukin 23 receptor helper type 1 ifn-γ chapter log regulates differentiation

Schema {🗺️}

ScholarlyArticle:
      headline:In Vitro Th Differentiation Protocol
      pageEnd:191
      pageStart:183
      image:https://media.springernature.com/w153/springer-static/cover/book/978-1-4939-2966-5.jpg
      genre:
         Springer Protocols
      isPartOf:
         name:TGF-β Signaling
         isbn:
            978-1-4939-2966-5
            978-1-4939-2965-8
         type:Book
      publisher:
         name:Springer New York
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Takashi Sekiya
            affiliation:
                  name:Keio University School of Medicine
                  address:
                     name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Akihiko Yoshimura
            affiliation:
                  name:Keio University School of Medicine
                  address:
                     name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
      keywords:Cytokines, Helper T cell subsets, TGF-β, IL-12, IL-23
      description:CD4+ T cells play central roles in adaptive immunity, driving appropriate immune responses to invading pathogens of diverse types. Four major CD4+ T cell subsets, Th1, Th2, Th17, and Treg cells are differentiated from naïve CD4+ T cells upon ligation of their T cell receptors with antigens, depending on the cytokines they receive. Th1 cells, which are induced by IL-12 and IFN-γ, mediate host defense against intracellular pathogens by exclusively expressing IFN-γ. Th2 cells, which are induced by IL4, secrete IL-4, IL-5, and IL-13, and protect hosts from helminths. IL-6 plus TGF-β induces Th17 cells, another Th subset identified relatively recently, express IL-17 and play important roles in the eradication of extracellular bacteria and fungi. Treg cells, which play central roles in immune suppression, are composed of either thymus-derived Treg cells (tTreg cells), which are directly developed from CD4-single positive (CD4-SP) cells in the thymus, or peripherally derived Treg cells (pTreg cells), which are induced by TGF-β plus IL-2 from naïve CD4+ T cells. Although the regulated induction of Th cells results in proper eradication of pathogens, their excess activation results in various immune-associated diseases. For example, aberrant activation of Th1 and Th17 has been implicated in autoimmune diseases, excess Th2 activity causes atopic diseases, and impaired function of Treg cells due to abrogation of Foxp3 has been shown to cause fatal inflammatory disorders both in human and in mouse. The methods for in vitro differentiation of each Th subset described above are presented here. We hope these methods will facilitate understanding of differentiation and function of CD4+ T cells and pathogenesis of various inflammatory diseases.
      datePublished:2016
      isAccessibleForFree:
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Book:
      name:TGF-β Signaling
      isbn:
         978-1-4939-2966-5
         978-1-4939-2965-8
Organization:
      name:Springer New York
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:Keio University School of Medicine
      address:
         name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
         type:PostalAddress
      name:Keio University School of Medicine
      address:
         name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Takashi Sekiya
      affiliation:
            name:Keio University School of Medicine
            address:
               name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Akihiko Yoshimura
      affiliation:
            name:Keio University School of Medicine
            address:
               name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
      name:Department of Microbiology and Immunology, Keio University School of Medicine, Shinjyuku-ku, Tokyo, Japan
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