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frequency, cells, patients, sle, cell, cdcdcdro, pubmed, treg, article, google, scholar, cas, cdcd, disease, foxp, figure, regulatory, controls, ctla, relatives, gene, tgfβ, lupus, population, activity, central, function, genetic, test, results, control, systemic, pbmc, genes, total, autoimmune, found, expression, erythematosus, significantly, females, production, study, trait, lower, table, authors, families, blood, marker,

Topics {✒️}

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         headline:Low frequency of CD4+CD25+ Treg in SLE patients: a heritable trait associated with CTLA4 and TGFβ gene variants
         description:CD4+CD25+ regulatory T cells play an essential role in maintaining immune homeostasis and preventing autoimmunity. Therefore, defects in Treg development, maintenance or function have been associated with several human autoimmune diseases including Systemic Lupus Erythematosus (SLE), a systemic autoimmune disease characterized by loss of tolerance to nuclear components and significantly more frequent in females. To investigate the involvement of Treg in SLE pathogenesis, we determined the frequency of CD4+CD25+CD45RO+ T cells, which encompass the majority of Treg activity, in the PBMC of 148 SLE patients (76 patients were part of 54 families), 166 relatives and 117 controls. SLE patients and their relatives were recruited in several Portuguese hospitals and through the Portuguese Lupus Association. Control individuals were blood donors recruited from several regional blood donor centers. Treg frequency was significantly lower in SLE patients than healthy controls (z = -6.161, P < 0.00001) and intermediate in the relatives' group. Remarkably, this T cell subset was also lower in females, most strikingly in the control population (z = 4.121, P < 0.001). We further ascertained that the decreased frequency of Treg in SLE patients resulted from the specific reduction of bona fide FOXP3+CD4+CD25+ Treg. Treg frequency was negatively correlated with SLE activity index (SLEDAI) and titers of serum anti-dsDNA antibodies. Both Treg frequency and disease activity were modulated by IVIg treatment in a documented SLE case. The segregation of Treg frequency within the SLE families was indicative of a genetic trait. Candidate gene analysis revealed that specific variants of CTLA4 and TGFβ were associated with the decreased frequency of Treg in PBMC, while FOXP3 gene variants were associated with affection status, but not with Treg frequency. SLE patients have impaired Treg production or maintenance, a trait strongly associated with SLE disease activity and autoantibody titers, and possibly resulting from the inability to convert FOXP3+CD25- into FOXP3+CD25+ T cells. Treg frequency is highly heritable within SLE families, with specific variants of the CTLA4 and TGFβ genes contributing to this trait, while FOXP3 contributes to SLE through mechanisms not involving a modulation of Treg frequency. These findings establish that the genetic components in SLE pathogenesis include genes related to Treg generation or maintenance.
         datePublished:2009-01-27T00:00:00Z
         dateModified:2009-01-27T00:00:00Z
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            Systemic Lupus Erythematosus Patient
            Treg Cell
            Cell Frequency
            FOXP3 Gene
            Immunology
            Allergology
            Vaccine
            Cytokines and Growth Factors
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      headline:Low frequency of CD4+CD25+ Treg in SLE patients: a heritable trait associated with CTLA4 and TGFβ gene variants
      description:CD4+CD25+ regulatory T cells play an essential role in maintaining immune homeostasis and preventing autoimmunity. Therefore, defects in Treg development, maintenance or function have been associated with several human autoimmune diseases including Systemic Lupus Erythematosus (SLE), a systemic autoimmune disease characterized by loss of tolerance to nuclear components and significantly more frequent in females. To investigate the involvement of Treg in SLE pathogenesis, we determined the frequency of CD4+CD25+CD45RO+ T cells, which encompass the majority of Treg activity, in the PBMC of 148 SLE patients (76 patients were part of 54 families), 166 relatives and 117 controls. SLE patients and their relatives were recruited in several Portuguese hospitals and through the Portuguese Lupus Association. Control individuals were blood donors recruited from several regional blood donor centers. Treg frequency was significantly lower in SLE patients than healthy controls (z = -6.161, P < 0.00001) and intermediate in the relatives' group. Remarkably, this T cell subset was also lower in females, most strikingly in the control population (z = 4.121, P < 0.001). We further ascertained that the decreased frequency of Treg in SLE patients resulted from the specific reduction of bona fide FOXP3+CD4+CD25+ Treg. Treg frequency was negatively correlated with SLE activity index (SLEDAI) and titers of serum anti-dsDNA antibodies. Both Treg frequency and disease activity were modulated by IVIg treatment in a documented SLE case. The segregation of Treg frequency within the SLE families was indicative of a genetic trait. Candidate gene analysis revealed that specific variants of CTLA4 and TGFβ were associated with the decreased frequency of Treg in PBMC, while FOXP3 gene variants were associated with affection status, but not with Treg frequency. SLE patients have impaired Treg production or maintenance, a trait strongly associated with SLE disease activity and autoantibody titers, and possibly resulting from the inability to convert FOXP3+CD25- into FOXP3+CD25+ T cells. Treg frequency is highly heritable within SLE families, with specific variants of the CTLA4 and TGFβ genes contributing to this trait, while FOXP3 contributes to SLE through mechanisms not involving a modulation of Treg frequency. These findings establish that the genetic components in SLE pathogenesis include genes related to Treg generation or maintenance.
      datePublished:2009-01-27T00:00:00Z
      dateModified:2009-01-27T00:00:00Z
      pageStart:1
      pageEnd:14
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1471-2172-10-5
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         Systemic Lupus Erythematosus
         Systemic Lupus Erythematosus Patient
         Treg Cell
         Cell Frequency
         FOXP3 Gene
         Immunology
         Allergology
         Vaccine
         Cytokines and Growth Factors
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            name:Instituto Gulbenkian de Ciência
            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
               type:PostalAddress
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      name:Ricardo C Ferreira
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            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
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      name:Lara Lourenço
      affiliation:
            name:Instituto Gulbenkian de Ciência
            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
               type:PostalAddress
            type:Organization
      name:Maria F Moraes-Fontes
      affiliation:
            name:Instituto Gulbenkian de Ciência
            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
               type:PostalAddress
            type:Organization
      name:Eugénia Santos
      affiliation:
            name:Associação dos Doentes com Lupus
            address:
               name:Associação dos Doentes com Lupus, Lisboa, Portugal
               type:PostalAddress
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            name:Hospital de Santa Maria
            address:
               name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
               type:PostalAddress
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      name:Miguel Alves
      affiliation:
            name:Hospital de Santa Maria
            address:
               name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
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      name:Cláudia Carvalho
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            name:Instituto de Ciências Biomédicas Abel Salazar
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               name:Instituto de Ciências Biomédicas Abel Salazar, Porto, Portugal
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      name:Berta Martins
      affiliation:
            name:Instituto de Ciências Biomédicas Abel Salazar
            address:
               name:Instituto de Ciências Biomédicas Abel Salazar, Porto, Portugal
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            name:Instituto Nacional de Saúde Dr. Ricardo Jorge
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            address:
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               type:PostalAddress
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      name:Carlos Vasconcelos
      affiliation:
            name:Associação dos Doentes com Lupus
            address:
               name:Associação dos Doentes com Lupus, Lisboa, Portugal
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            address:
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               type:PostalAddress
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      affiliation:
            name:Associação dos Doentes com Lupus
            address:
               name:Associação dos Doentes com Lupus, Lisboa, Portugal
               type:PostalAddress
            type:Organization
            name:Hospital de Santa Maria
            address:
               name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
               type:PostalAddress
            type:Organization
      name:Jocelyne Demengeot
      affiliation:
            name:Instituto Gulbenkian de Ciência
            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
               type:PostalAddress
            type:Organization
      name:Astrid M Vicente
      affiliation:
            name:Instituto Gulbenkian de Ciência
            address:
               name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
               type:PostalAddress
            type:Organization
            name:Instituto Nacional de Saúde Dr. Ricardo Jorge
            address:
               name:Instituto Nacional de Saúde Dr. Ricardo Jorge, Lisboa, Portugal
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Associação dos Doentes com Lupus, Lisboa, Portugal
      name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
      name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
      name:Instituto de Ciências Biomédicas Abel Salazar, Porto, Portugal
      name:Instituto de Ciências Biomédicas Abel Salazar, Porto, Portugal
      name:Instituto Nacional de Saúde Dr. Ricardo Jorge, Porto, Portugal
      name:Associação dos Doentes com Lupus, Lisboa, Portugal
      name:Associação dos Doentes com Lupus, Lisboa, Portugal
      name:Associação dos Doentes com Lupus, Lisboa, Portugal
      name:Hospital Divino Espírito Santo de Ponta Delgada, EPE, Ponta Delgada, Portugal
      name:Associação dos Doentes com Lupus, Lisboa, Portugal
      name:Clínica Universitária de Medicina II, Hospital de Santa Maria, Lisboa, Portugal
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Instituto Gulbenkian de Ciência, Oeiras, Portugal
      name:Instituto Nacional de Saúde Dr. Ricardo Jorge, Lisboa, Portugal

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