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Publication Detail
IL-12p35 subunit contributes to autoimmunity by limiting IL-27-driven regulatory responses.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Vasconcellos R, Carter NA, Rosser EC, Mauri C
  • Publication date:
  • Pagination:
    3402, 3412
  • Journal:
    J Immunol
  • Volume:
  • Issue:
  • Status:
  • Country:
    United States
  • PII:
  • Language:
  • Keywords:
    Animals, Arthritis, Experimental, Autoimmunity, B-Lymphocytes, Cell Differentiation, Cell Separation, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Interleukin-12 Subunit p35, Interleukins, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, T-Lymphocytes, Regulatory
Contrasting results have emerged from studies performed using IL-12p35(-/-) mice. Animals lacking the IL-12p35 subunit can either be protected from or develop exacerbated autoimmune diseases, intracellular infections, and delayed-type hypersensitivity responses. In this study, we report that mice lacking the IL-12p35 subunit develop a significantly milder Ag-induced arthritis compared with wild-type (WT) mice. Lack of severe inflammation is accompanied by an increase in the mRNA levels of the Ebi-3 and p28 subunits and increased secretion of IL-27 and IL-10. This anti-inflammatory environment contributed to increased differentiation of regulatory T and B cells with intact suppressive function. Furthermore, IL-12p35(-/-) mice display reduced numbers of Th17 cells compared with WT arthritic mice. Neutralization of IL-27, but not the systemic administration of IL-12, restored inflammation and Th17 to levels seen in WT mice. The restoration of disease phenotype after anti-IL-27 administration indicates that the IL-12p35 subunit acts as negative regulator of the developing IL-27 response in this model of arthritis.
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