Inhaltszusammenfassung

Regulatory CD4( )CD25( ) T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact-mediated suppression of conventional CD4( ) T cells by human CD25( ) Treg cells is fixation resistant, independent from membrane-bound TGF-beta but requires activation and protein synthesis of CD25( ) Treg cells. Coactivation of CD25( ) Treg cells with Treg cell-depleted CD4( ) T cells results in anergized CD4( ) T cells that in turn inhibit the activatio...Regulatory CD4( )CD25( ) T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact-mediated suppression of conventional CD4( ) T cells by human CD25( ) Treg cells is fixation resistant, independent from membrane-bound TGF-beta but requires activation and protein synthesis of CD25( ) Treg cells. Coactivation of CD25( ) Treg cells with Treg cell-depleted CD4( ) T cells results in anergized CD4( ) T cells that in turn inhibit the activation of conventional, freshly isolated CD4( ) T helper (Th) cells. This infectious suppressive activity, transferred from CD25( ) Treg cells via cell contact, is cell contact-independent and partially mediated by soluble transforming growth factor (TGF)-beta. The induction of suppressive properties in conventional CD4( ) Th cells represents a mechanism underlying the phenomenon of infectious tolerance. This explains previously published conflicting data on the role of TGF-beta in CD25( ) Treg cell-induced immunosuppression.» weiterlesen» einklappen

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Klassifikation

DFG Fachgebiet:
2.21 - Mikrobiologie, Virologie und Immunologie

DDC Sachgruppe:
Medizin