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Engagement of distinct epitopes on CD43 induces different co-stimulatory pathways in human T cells
Verfasser / VerfasserinStöckl, Johannes ; Strobl, Herbert ; Zlabinger, Gerhard J. ; Steinberger, Peter ; Gerwien, Jens G. ; Puck, Alexander ; Jutz, Sabrina ; Cejka, Petra ; Modak, Madhura ; Majdic, Otto
Erschienen in
Immunology, Hoboken, 2016, Jg. 149, H. 3, S. 280-296
ErschienenHoboken : Wiley-Blackwell, 2016
DokumenttypAufsatz in einer Zeitschrift
Schlagwörter (EN)cd43 / co-stimulation / heterotypic cell adhesion / suppressor t cells / t-cell polarization / wiskott-aldrich syndrome / nf-kappa-b / dendritic cells / in-vitro / sialophorin cd43 / cutting edge / major sialoglycoprotein / surface glycoprotein / monoclonal-antibody / cytokine production
Projekt-/ReportnummerP 22869-B11
URNurn:nbn:at:at-ubmuw:3-1469 Persistent Identifier (URN)
 Das Werk ist frei verfügbar
Engagement of distinct epitopes on CD43 induces different co-stimulatory pathways in human T cells [1.4 mb]
Zusammenfassung (Englisch)

Co-receptors, being either co-stimulatory or co-inhibitory, play a pivotal role in T-cell immunity. Several studies have indicated that CD43, one of the abundant T-cell surface glycoproteins, acts not only as a potent co-receptor but also as a negative regulator for T-cell activation. Here we demonstrate that co-stimulation of human peripheral blood (PB) T cells through two distinct CD43 epitopes recognized by monoclonal antibodies (mAb) CD43-6E5 (T6E5-act) and CD43-10G7 (T10G7-act) potently induced T-cell proliferation. However, T-cell co-stimulation through two CD43 epitopes differentially regulated activation of nuclear factor of activated T cells (NFAT) and nuclear factor-kappa B (NF-kappa B) transcription factors, T-cell cytokine production and effector function. T6E5-act produced high levels of interleukin-22 (IL-22) and interferon-gamma (IFN-gamma) similar to T cells activated via CD28 (TCD28-act), whereas T10G7-act produced low levels of inflammatory cytokines but higher levels of regulatory cytokines transforming growth factor-beta (TGF-beta) and interleukin-35 (IL-35). Compared with T6E5-act or to TCD28-act, T10G7-act performed poorly in response to re-stimulation and further acquired a T-cell suppressive function. T10G7-act did not directly inhibit proliferation of responder T cells, but formed stable heterotypic clusters with dendritic cells (DC) via CD2 to constrain activation of responder T cells. Together, our data demonstrate that CD43 is a unique and polarizing regulator of T-cell function.

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