We are analyzing https://link.springer.com/article/10.1186/s12865-015-0111-2.

Title:
IFNγ+ Treg in-vivo and in-vitro represent both activated nTreg and peripherally induced aTreg and remain phenotypically stable in-vitro after removal of the stimulus | BMC Immunology
Description:
Background IFNγ-producing CD4+CD25+Foxp3+CD127- Treg represent the first line of Treg during an immune response. In the present study we determined whether IFNγ+ Treg in-vivo and in-vitro are Helios-positive representing activated natural (nTreg) or Helios-negative representing adaptive Treg (aTreg) and whether they originate from CD4+CD25+ and/or CD4+CD25- PBL. Furtheron, we investigated whether they are inducible by recombinant IFNγ (rIFNγ) as a single stimulus, decrease in-vitro after elimination of the stimulus, and have a demethylated Foxp3 Treg-specific demethylated region (TSDR) which is associated with stable Foxp3 expression. Method Subsets of IFNγ+ Treg were determined in peripheral blood of healthy controls using eight-color flow cytometry and were further investigated in-vitro. Foxp3 TSDR methylation status was determined using bisulphite polymerase chain reaction (PCR) and high resolution melt (HRM) analysis. Results Nearly all Treg in the peripheral blood were Helios+IFNγ- (1.9 ± 1.1/μl) and only few were Helios+IFNγ+ or Helios-IFNγ+ Treg (both 0.1 ± 0.1/μl). Enriched IFNγ+ Treg subsets showed in part strong Foxp3 TSDR demethylation. In-vitro, rIFNγ was unable to induce Treg. CD4+CD25+ enriched PBL stimulated with PMA/Ionomycin in the presence of rIFNγ were rather resistant to the effect of rIFNγ, in contrast to CD4+CD25- enriched PBL which showed increasing total Treg with Helios+ Treg switching from IFNγ- to IFNγ+ and increasing Helios-IFNγ+ Treg. The data indicate that rIFNγ, in combination with a polyclonal stimulus, activates nTreg and induces aTreg. When phorbol 12-myristate 13-acetate (PMA)/Ionomycin was washed out from the cell culture after 6 h stimulation, Treg induction continued for at least 96 h of cell culture, contradicting the hypothesis that removal of the stimulus results in significant decrease of IFNγ- and IFNγ+ CD4+CD25+Foxp3+CD127- Treg due to loss of Foxp3 expression. Conclusions IFNγ+Helios- aTreg as well as IFNγ+Helios+ nTreg are detectable in the blood of healthy individuals, show in part strong Foxp3 TSDR demethylation and are inducible in-vitro. The present data provide further insight concerning the in-vivo and in-vitro characteristics of IFNγ+ Treg and help to understand their role in immunoregulation. Alloantigen-specific demethylated IFNγ+Helios+ nTreg might represent a suitable marker for monitoring graft-specific immunosuppression in renal transplant recipients.
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Keywords {🔍}

treg, ifnγ, pbl, foxp, cells, cell, rifnγ, cdcd, pubmed, heliosifnγ, article, ntreg, ngml, enriched, google, scholar, healthy, data, tsdr, helios, invitro, cas, expression, dna, stimulus, preparations, cdcdfoxpcd, resp, immunol, blood, methylation, regulatory, pmaiono, fig, induced, atreg, subsets, cdcdcdifnγ, individuals, activated, pmaionomycin, central, stimulated, separated, lymphocytes, cultures, increase, min, buffer, analysis,

Topics {✒️}

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Questions {❓}

Do Natural T Regulatory Cells become Activated to Antigen Specific T Regulatory Cells in Transplantation and in Autoimmunity?
How are T(H)1 and T(H)2 effector cells made?
However, what is the fate of IFNγ+ Treg when the immune response is stopped?

Schema {🗺️}

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         headline:IFNγ+ Treg in-vivo and in-vitro represent both activated nTreg and peripherally induced aTreg and remain phenotypically stable in-vitro after removal of the stimulus
         description:IFNγ-producing CD4+CD25+Foxp3+CD127- Treg represent the first line of Treg during an immune response. In the present study we determined whether IFNγ+ Treg in-vivo and in-vitro are Helios-positive representing activated natural (nTreg) or Helios-negative representing adaptive Treg (aTreg) and whether they originate from CD4+CD25+ and/or CD4+CD25- PBL. Furtheron, we investigated whether they are inducible by recombinant IFNγ (rIFNγ) as a single stimulus, decrease in-vitro after elimination of the stimulus, and have a demethylated Foxp3 Treg-specific demethylated region (TSDR) which is associated with stable Foxp3 expression. Subsets of IFNγ+ Treg were determined in peripheral blood of healthy controls using eight-color flow cytometry and were further investigated in-vitro. Foxp3 TSDR methylation status was determined using bisulphite polymerase chain reaction (PCR) and high resolution melt (HRM) analysis. Nearly all Treg in the peripheral blood were Helios+IFNγ- (1.9 ± 1.1/μl) and only few were Helios+IFNγ+ or Helios-IFNγ+ Treg (both 0.1 ± 0.1/μl). Enriched IFNγ+ Treg subsets showed in part strong Foxp3 TSDR demethylation. In-vitro, rIFNγ was unable to induce Treg. CD4+CD25+ enriched PBL stimulated with PMA/Ionomycin in the presence of rIFNγ were rather resistant to the effect of rIFNγ, in contrast to CD4+CD25- enriched PBL which showed increasing total Treg with Helios+ Treg switching from IFNγ- to IFNγ+ and increasing Helios-IFNγ+ Treg. The data indicate that rIFNγ, in combination with a polyclonal stimulus, activates nTreg and induces aTreg. When phorbol 12-myristate 13-acetate (PMA)/Ionomycin was washed out from the cell culture after 6 h stimulation, Treg induction continued for at least 96 h of cell culture, contradicting the hypothesis that removal of the stimulus results in significant decrease of IFNγ- and IFNγ+ CD4+CD25+Foxp3+CD127- Treg due to loss of Foxp3 expression. IFNγ+Helios- aTreg as well as IFNγ+Helios+ nTreg are detectable in the blood of healthy individuals, show in part strong Foxp3 TSDR demethylation and are inducible in-vitro. The present data provide further insight concerning the in-vivo and in-vitro characteristics of IFNγ+ Treg and help to understand their role in immunoregulation. Alloantigen-specific demethylated IFNγ+Helios+ nTreg might represent a suitable marker for monitoring graft-specific immunosuppression in renal transplant recipients.
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         dateModified:2015-08-13T00:00:00Z
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            Foxp3 TSDR demethylation
            IFNγ
            Th1
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            Allergology
            Vaccine
            Cytokines and Growth Factors
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         IFNγ+ aTreg
         Foxp3 TSDR demethylation
         IFNγ
         Th1
         Healthy individuals
         Immunology
         Allergology
         Vaccine
         Cytokines and Growth Factors
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      name:Karina Trojan
      affiliation:
            name:Institute of Immunology, University Hospital Heidelberg
            address:
               name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany
               type:PostalAddress
            type:Organization
      name:Martina Adamek
      affiliation:
            name:Institute of Immunology, University Hospital Heidelberg
            address:
               name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany
               type:PostalAddress
            type:Organization
      name:Gerhard Opelz
      affiliation:
            name:Institute of Immunology, University Hospital Heidelberg
            address:
               name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany
               type:PostalAddress
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      name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany
      name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany
      name:Department of Transplantation-Immunology, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany

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