Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0014070 (
encephalomyelitis
)
13,017
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Single-nucleotide polymorphisms close to
IL22RA2
, coding for the soluble interleukin (IL)-22-binding protein (
IL-22BP
), are strongly and reproducibly associated with multiple sclerosis (MS), but there is little data on how this molecule may affect neuroinflammation. Here, we have studied the mouse ortholog in C57BL/6 wild-type and Il22ra2-deficient mice in the context of experimental autoimmune
encephalomyelitis
(myelin oligodendrocyte glycoprotein-EAE). In wild-type mice, we demonstrated changes in the levels of transcripts for IL-22, the signaling IL-22 receptor and
IL-22BP
in lymphoid tissues at the time of T-cell priming and in the inflamed central nervous system (CNS). Because
IL-22BP
is known to antagonize IL-22 signaling, a primarily pro-inflammatory cytokine, we hypothesized that the Il22ra2-deficient mice would have more severe EAE. Paradoxically, the knockout mice displayed a less severe disease course, less demyelination and less infiltration of immune cells in the CNS. The most straightforward interpretation of our findings is that lack of
IL-22BP
leads to a higher availability of IL-22, which in the case of CNS inflammation, surprisingly acts in a protective fashion. Thus, deletion of the ortholog of the MS risk gene Il22ra2 in mice has beneficial effects on EAE, which may be considered in new therapeutic strategies for treating neuroinflammation.
...
PMID:The multiple sclerosis risk gene IL22RA2 contributes to a more severe murine autoimmune neuroinflammation. 2500 63
