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Th17 pathway genes are primarily downregulated by spinal cord injury (729.4)
Author(s) -
Jones T Bucky,
Jones Carleton
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.729.4
Subject(s) - neuroinflammation , immunology , rar related orphan receptor gamma , innate immune system , multiple sclerosis , acquired immune system , downregulation and upregulation , spinal cord injury , biology , interleukin 17 , microbiology and biotechnology , gene , medicine , inflammation , spinal cord , immune system , neuroscience , genetics , foxp3
Spinal cord injury (SCI) elicits a neuroinflammatory response involving cells of both innate and adaptive immunity. A new subtype of T‐helper cells, Th17, plays a role in several neuroinflammatory pathologies including multiple sclerosis and stroke. We therefore examined the role of Th17 cells in neuroinflammation secondary to SCI. Quantitative reverse transcriptase‐polymerase chain reaction (qRT‐PCR) arrays were used to evaluate postinjury expression of 84 genes relating to the Th17 pathway in a rat model of SCI. At 7 days post injury (dpi) mRNAs of 18 genes were increased and 27 were decreased compared to controls. Of these, 4 genes remained up‐ and 15 downregulated at 28 dpi. Although the genes for TGF‐β1 and IL‐6, cytokines required for differentiation of Th17 cells, were both upregulated at 7 dpi this was not associated with increased IL‐17. Indeed, Rorc, IL‐17b, and IL‐17f mRNAs were all decreased while IL‐17a and IL‐17c mRNAs were unaffected by injury. This was perhaps because IL‐23a, required for the survival and proliferation of Th17 cells, was also decreased. Similar effects were observed at 28 dpi, although generally lesser in magnitude. Although Th17 cells and the IL‐17 family of cytokines mediate cross talk between adaptive and innate immunity in many pathologic conditions, our data do not support a role for this T‐cell subset in the chronic inflammatory response to SCI.