International archives of allergy and immunology · 2011
IL-17A and IL-17F expression in B lymphocytes.
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Vazquez-Tello Alejandro, Halwani Rabih, Li Rui, Nadigel Jessica, Bar-Or Amir, Mazer Bruce D, Eidelman David H, Al-Muhsen Saleh, Hamid Qutayba
Аннотация
BACKGROUND: Recent evidence suggests that cells other than Th-17 lymphocytes express interleukin (IL)-17A and IL-17F and contribute to the production of these cytokines in immunologically mediated diseases. B lymphocytes are known to be an important source of cytokines in chronic inflammatory diseases. We therefore investigated the potential of human B lymphocytes to produce IL-17A and IL-17F.
METHODS: Highly purified B cells were obtained using a multiple-step separation procedure which included rosette depletion, adherence depletion, CD3+ cell magnetic activated depletion and CD19+ magnetic activated positive cell selection. In these CD19+ B cell fractions, CD3+/CD4+ and CD14+ cells were negligible (<0.2%), and CD8 and CD161 mRNAs were undetectable. The CD19+/CD20+ B cells were stimulated with IL-4, interferon-γ, IL-6, IL-23 and transforming growth factor (TGF)-β, and the expression of IL-17A and IL-17F in response to stimulation was determined by quantitative reverse transcription (RT)-PCR, Western blot, immunocytochemistry and ELISA.
RESULTS: Evidence of expression of IL-17A and IL-17F in purified B cells was obtained using RT-PCR, flow cytometry, immunofluorescence microscopy, Western immunoblotting and ELISA. Stimulation of B cells with IL-6, IL-23 or TGF-β upregulated the expression of both IL-17A and F cytokines.
CONCLUSIONS: These novel findings provide evidence that cytokine-stimulated B lymphocytes could be a significant source of IL-17A and IL-17F and support the notion that these cells actively participate in immune responses via alternative mechanisms in addition to the classic release of antibodies.
METHODS: Highly purified B cells were obtained using a multiple-step separation procedure which included rosette depletion, adherence depletion, CD3+ cell magnetic activated depletion and CD19+ magnetic activated positive cell selection. In these CD19+ B cell fractions, CD3+/CD4+ and CD14+ cells were negligible (<0.2%), and CD8 and CD161 mRNAs were undetectable. The CD19+/CD20+ B cells were stimulated with IL-4, interferon-γ, IL-6, IL-23 and transforming growth factor (TGF)-β, and the expression of IL-17A and IL-17F in response to stimulation was determined by quantitative reverse transcription (RT)-PCR, Western blot, immunocytochemistry and ELISA.
RESULTS: Evidence of expression of IL-17A and IL-17F in purified B cells was obtained using RT-PCR, flow cytometry, immunofluorescence microscopy, Western immunoblotting and ELISA. Stimulation of B cells with IL-6, IL-23 or TGF-β upregulated the expression of both IL-17A and F cytokines.
CONCLUSIONS: These novel findings provide evidence that cytokine-stimulated B lymphocytes could be a significant source of IL-17A and IL-17F and support the notion that these cells actively participate in immune responses via alternative mechanisms in addition to the classic release of antibodies.