In vitro cytokine treatment of B cell defects in HIV-infected hemophilia patients

• Verfasst von: Weimer, Rolf [VerfasserIn]
• Verfasst von: Zipperle, Silvia [VerfasserIn]
• Verfasst von: Daniel, Volker [VerfasserIn]
• Verfasst von: Opelz, Gerhard [VerfasserIn]
• Titel: In vitro cytokine treatment of B cell defects in HIV-infected hemophilia patients
• Verf.angabe: Rolf Weimer, Silvia Zipperle, Volker Daniel, Gerhard Opelz
• E-Jahr: 1995
• Jahr: July 1995
• Umfang: 11 S.
• Fussnoten: Gesehen am 22.08.2024
• Titel Quelle: Enthalten in: Vox sanguinis
• Ort Quelle: Oxford [u.a.] : Wiley-Blackwell, 1956
• Jahr Quelle: 1995
• Band/Heft Quelle: 69(1995), 1, Seite 27-37
• ISSN Quelle: 1423-0410
• DOI: doi:10.1111/j.1423-0410.1995.tb00344.x
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1899376739

Abstract

HIV-infected patients exhibit defects in B cell differentiation and in the IL-6 response of B cells, in association with autoantibody formation against T cells. These autoantibodies have been implicated as important factors in the development of immunodeficiency disease. As the restoration of defective B cell responses might prevent autoantibody formation and the resulting immunosuppression, we studied whether in vitro treatment with recombinant IL-2 (rIL-2), recombinant IL-4 (rIL-4) or recombinant IL-6 (rIL-6) might restore the response of B cells of HIV-infected patients. B cells of 6 HIV-negative hemophilia patients, 4 HIV-positive patients at CDC stage II, III, 4 HIV-positive patients at CDC stage IV, and 6 healthy controls were tested in Staphylococcus aureus Cowan I (SAC-I)-stimulated B cell cultures and Pokeweed mitogen (PWM)-stimulated allogeneic B and T cell cocultures. B cell differentiation was assessed in a reverse hemolytic plaque assay and by ELISA determination of IgM, IgG and IL-6 in culture supernatants. In vitro application of rIL-6 resulted in suppression of both elevated unstimulated and mitogen-stimulated B cell responses in a dose-dependent manner which was in part due to feedback inhibition. PWM- and SAC-I-stimulated IgG and IgM responses, respectively, could be restored after addition of 10 U/ml rIL-2 in HIV-negative patients, but not in HIV-positive patients. Addition of rIL-4 to cultures resulted in suppression of both unstimulated and mitogen-stimulated IL-6 secretion and B cell responses. Severely depressed B cell responses in CDC IV patients were not significantly affected by cytokine application. These results indicate that defective Ig responses in HIV-negative patients may be restored by rIL-2 treatment whereas HIV-induced B cell defects are not corrected by supply of T cell help or cytokines promoting B cell growth and differentiation.