Autocrine Regulation of IL-12 Receptor Expression Is Independent of Secondary IFN-γ Secretion and not Restricted to T and NK Cells

التفاصيل البيبلوغرافية
العنوان: Autocrine Regulation of IL-12 Receptor Expression Is Independent of Secondary IFN-γ Secretion and not Restricted to T and NK Cells
المؤلفون: Deborah K. Thibodeaux, Sharon E. Hunter, Kristine E. Waldburger, Judy L. Bliss, William L. Trepicchio, Joseph P. Sypek, Kyriaki Dunussi-Joannopoulos, Samuel J. Goldman, John P. Leonard
المصدر: The Journal of Immunology. 163:5257-5264
بيانات النشر: The American Association of Immunologists, 1999.
سنة النشر: 1999
مصطلحات موضوعية: Immunology, Immunology and Allergy
الوصف: The biological response to IL-12 is mediated through specific binding to a high affinity receptor complex composed of at least two subunits (designated IL-12Rβ1 and IL-12Rβ2) that are expressed on NK cells and activated T cells. The selective loss of IL-12Rβ2 expression during Th2 T cell differentiation suggests that regulation of this receptor component may govern IL-12 responsiveness. In murine assays, down-regulation of IL-12Rβ2 expression can be prevented by treatment with IFN-γ, indicating that receptor expression and hence IL-12 responsiveness may be regulated, at least in part, by the local cytokine milieu. In this study, we report that cellular expression of both IL-12Rβ1 and β2 mRNA is increased in the lymph nodes of naive mice following systemic administration of murine rIL-12 (rmIL-12). Changes in IL-12R mRNA were associated with increased IFN-γ secretion following ex vivo activation of lymph node cells with rmIL-12, indicating the presence of a functional receptor complex. Expression of IL-12R mRNA was not restricted to lymph node T cells, and its autocrine regulation was independent of secondary IFN-γ secretion. Data from fractionated lymph node cells as well as rmIL-12-treated B cell-deficient mice suggest that IL-12-responsive B cells may represent an alternative cellular source for IFN-γ production. However, the strength of the biological response to rmIL-12 is not governed solely by receptor expression, as rmIL-12-induced IFN-γ secretion from cultured lymph node cells is accessory cell dependent and can be partially blocked by inhibition of B7 costimulation.
تدمد: 1550-6606
0022-1767
DOI: 10.4049/jimmunol.163.10.5257
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::54c6b597cbaccce9c8b0a3fcfa1f41da
https://doi.org/10.4049/jimmunol.163.10.5257
رقم الانضمام: edsair.doi...........54c6b597cbaccce9c8b0a3fcfa1f41da
قاعدة البيانات: OpenAIRE
الوصف
تدمد:15506606
00221767
DOI:10.4049/jimmunol.163.10.5257