| First Author | Huard A | Year | 2021 |
| Journal | J Immunol | Volume | 206 |
| Issue | 5 | Pages | 1058-1066 |
| PubMed ID | 33504620 | Mgi Jnum | J:303890 |
| Mgi Id | MGI:6515402 | Doi | 10.4049/jimmunol.2000923 |
| Citation | Huard A, et al. (2021) IL-38 Ablation Reduces Local Inflammation and Disease Severity in Experimental Autoimmune Encephalomyelitis. J Immunol 206(5):1058-1066 |
| abstractText | IL-38 is an IL-1 family receptor antagonist that restricts IL-17-driven inflammation by limiting cytokine production from macrophages and T cells. In the current study, we aimed to explore its role in experimental autoimmune encephalomyelitis in mice, which is, among others, driven by IL-17. Unexpectedly, IL-38-deficient mice showed strongly reduced clinical scores and histological markers of experimental autoimmune encephalomyelitis. This was accompanied by reduced inflammatory cell infiltrates, including macrophages and T cells, as well as reduced expression of inflammatory markers in the spinal cord. IL-38 was highly expressed by infiltrating macrophages in the spinal cord, and in vitro activated IL-38-deficient bone marrow-derived macrophages showed reduced expression of inflammatory markers, accompanied by altered cellular metabolism. These data suggest an alternative cell-intrinsic role of IL-38 to promote inflammation in the CNS. |
