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We are analyzing https://link.springer.com/article/10.1186/1471-2172-10-56.

Title:
The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection | BMC Immunology
Description:
Background Leukocyte Ig-like receptors (LILR) are a family of innate immune receptors with immunomodulatory functions. High-level expression of the receptors LILRB2 (ILT4) and LILRB4 (ILT3) is a feature of tolerogenic antigen presenting cells and has been observed in cancer and transplant situations. There are relatively few studies regarding these receptors in the context of infection and it is not yet clear how LILRB4 exerts its inhibitory effects. Results We studied the effects of LILRB4 ligation on antigen presenting cell phenotype, and the expression of LILRB2 and LILRB4 on Salmonella- infected antigen presenting cells. Ligation of LILRB4 throughout in vitro culture of dendritic cells led to an upregulation of the co-stimulatory protein CD86. Alterations in the production of IL-8 and IL-10 by LILRB4-ligated macrophages were also observed. Infection with Salmonella typhimurium or TLR stimulation with Salmonella components led to an upregulation of LILRB2 and LILRB4. Conclusion Our results indicate that the inhibitory effects of LILRB4 do not result from a failure to upregulate co-stimulatory proteins. In addition to the high level expression that can render antigen presenting cells tolerogenic, there may be a role for lower level expression and activity of LILRB2 and LILRB4 in response to TLR signalling during an immune response to bacterial infection.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
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Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 7,626,182 visitors per month in the current month.

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How Does Link.springer.com Make Money? {πŸ’Έ}

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Keywords {πŸ”}

lilrb, cells, article, cell, pubmed, expression, dendritic, google, scholar, antigen, presenting, cas, salmonella, immune, ilt, inhibitory, receptor, infection, macrophages, response, receptors, figure, ligation, lps, lilr, effects, culture, tlr, performed, typhimurium, analysis, innate, cultured, immunol, authors, observed, upregulation, cytokine, phenotype, studies, results, isotype, control, human, flow, antibody, protein, role, surface, treatment,

Topics {βœ’οΈ}

alloantigen specific cd8+cd28-foxp3+ cytokine secretion profile disease-modifying anti-rheumatic drugs real-time pcr assay nicolas lapaque mixed leukocyte reactions open access article full size image il-10 inhibits endothelium-dependent hu-nod/scid mice article download pdf lilr expression profile assess cytokine profiles real-time pcr monocyte-derived dendritic cells receptor-induced interferon production infected monocyte-derived macrophages infect monocyte-derived macrophages similar expression profiles lilrb4-ligated dendritic cells antigen presenting cell lps-matured dendritic cells il-10-induced dendritic cells innate/adaptive immune regulation aspirin-treated human dcs leukaemia research fund monocyte-derived macrophages treated vitro-cultured dendritic cells cell-cell contact antigen presenting cells tolerogenic dendritic cells typhimurium previously heat-killed 50 ng/ml m-csf dendritic cell stimulators privacy choices/manage cookies innate immune cells human dendritic cells full access arthritis research campaign authors’ original file cytokine bead array manavalan js dendritic cells led dendritic cells involved dendritic cells resulting innate immune receptors cell-surface phenotype immune inhibitory nature monocyte-derived macrophages cell surface markers

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection
         description:Leukocyte Ig-like receptors (LILR) are a family of innate immune receptors with immunomodulatory functions. High-level expression of the receptors LILRB2 (ILT4) and LILRB4 (ILT3) is a feature of tolerogenic antigen presenting cells and has been observed in cancer and transplant situations. There are relatively few studies regarding these receptors in the context of infection and it is not yet clear how LILRB4 exerts its inhibitory effects. We studied the effects of LILRB4 ligation on antigen presenting cell phenotype, and the expression of LILRB2 and LILRB4 on Salmonella- infected antigen presenting cells. Ligation of LILRB4 throughout in vitro culture of dendritic cells led to an upregulation of the co-stimulatory protein CD86. Alterations in the production of IL-8 and IL-10 by LILRB4-ligated macrophages were also observed. Infection with Salmonella typhimurium or TLR stimulation with Salmonella components led to an upregulation of LILRB2 and LILRB4. Our results indicate that the inhibitory effects of LILRB4 do not result from a failure to upregulate co-stimulatory proteins. In addition to the high level expression that can render antigen presenting cells tolerogenic, there may be a role for lower level expression and activity of LILRB2 and LILRB4 in response to TLR signalling during an immune response to bacterial infection.
         datePublished:2009-10-27T00:00:00Z
         dateModified:2009-10-27T00:00:00Z
         pageStart:1
         pageEnd:9
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1471-2172-10-56
         keywords:
            Dendritic Cell
            Antigen Present Cell
            Innate Immune Receptor
            Mixed Leukocyte Reaction
            Cytokine Secretion Profile
            Immunology
            Allergology
            Vaccine
            Cytokines and Growth Factors
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                     name:NorthWestern University
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                        name:NorthWestern University, Evanston, USA
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               name:John Trowsdale
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                     name:St Georges, University of London
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                        name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK
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ScholarlyArticle:
      headline:The inhibitory receptor LILRB4 (ILT3) modulates antigen presenting cell phenotype and, along with LILRB2 (ILT4), is upregulated in response to Salmonella infection
      description:Leukocyte Ig-like receptors (LILR) are a family of innate immune receptors with immunomodulatory functions. High-level expression of the receptors LILRB2 (ILT4) and LILRB4 (ILT3) is a feature of tolerogenic antigen presenting cells and has been observed in cancer and transplant situations. There are relatively few studies regarding these receptors in the context of infection and it is not yet clear how LILRB4 exerts its inhibitory effects. We studied the effects of LILRB4 ligation on antigen presenting cell phenotype, and the expression of LILRB2 and LILRB4 on Salmonella- infected antigen presenting cells. Ligation of LILRB4 throughout in vitro culture of dendritic cells led to an upregulation of the co-stimulatory protein CD86. Alterations in the production of IL-8 and IL-10 by LILRB4-ligated macrophages were also observed. Infection with Salmonella typhimurium or TLR stimulation with Salmonella components led to an upregulation of LILRB2 and LILRB4. Our results indicate that the inhibitory effects of LILRB4 do not result from a failure to upregulate co-stimulatory proteins. In addition to the high level expression that can render antigen presenting cells tolerogenic, there may be a role for lower level expression and activity of LILRB2 and LILRB4 in response to TLR signalling during an immune response to bacterial infection.
      datePublished:2009-10-27T00:00:00Z
      dateModified:2009-10-27T00:00:00Z
      pageStart:1
      pageEnd:9
      license:https://creativecommons.org/licenses/by/2.0
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      keywords:
         Dendritic Cell
         Antigen Present Cell
         Innate Immune Receptor
         Mixed Leukocyte Reaction
         Cytokine Secretion Profile
         Immunology
         Allergology
         Vaccine
         Cytokines and Growth Factors
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                  address:
                     name:Department of Pathology, Cambridge University, Cambridge, UK
                     type:PostalAddress
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                  name:Cambridge University
                  address:
                     name:Department of Pathology, Cambridge University, Cambridge, UK
                     type:PostalAddress
                  type:Organization
                  name:NorthWestern University
                  address:
                     name:NorthWestern University, Evanston, USA
                     type:PostalAddress
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            type:Person
            name:John Trowsdale
            affiliation:
                  name:Cambridge University
                  address:
                     name:Department of Pathology, Cambridge University, Cambridge, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Rachel L Allen
            affiliation:
                  name:St Georges, University of London
                  address:
                     name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK
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      name:Damien P Brown
      affiliation:
            name:Cambridge University
            address:
               name:Department of Pathology, Cambridge University, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Des C Jones
      affiliation:
            name:Cambridge University
            address:
               name:Department of Pathology, Cambridge University, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Katie J Anderson
      affiliation:
            name:St Georges, University of London
            address:
               name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK
               type:PostalAddress
            type:Organization
      name:Nicolas Lapaque
      affiliation:
            name:Cambridge University
            address:
               name:Department of Pathology, Cambridge University, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Robin A Buerki
      affiliation:
            name:Cambridge University
            address:
               name:Department of Pathology, Cambridge University, Cambridge, UK
               type:PostalAddress
            type:Organization
            name:NorthWestern University
            address:
               name:NorthWestern University, Evanston, USA
               type:PostalAddress
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      name:John Trowsdale
      affiliation:
            name:Cambridge University
            address:
               name:Department of Pathology, Cambridge University, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Rachel L Allen
      affiliation:
            name:St Georges, University of London
            address:
               name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pathology, Cambridge University, Cambridge, UK
      name:Department of Pathology, Cambridge University, Cambridge, UK
      name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK
      name:Department of Pathology, Cambridge University, Cambridge, UK
      name:Department of Pathology, Cambridge University, Cambridge, UK
      name:NorthWestern University, Evanston, USA
      name:Department of Pathology, Cambridge University, Cambridge, UK
      name:Centre for Infection, Division of Cellular and Molecular Medicine, St Georges, University of London, London, UK

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