IL-38 Ablation Reduces Local Inflammation and Disease Severity in Experimental Autoimmune Encephalomyelitis

被引：17

作者：

Huard, Arnaud ^{[1
]}

Hoai Nam Do ^{[1
]}

Frank, Ann-Christin ^{[1
]}

Sirait-Fischer, Evelyn ^{[1
]}

Fuhrmann, Dominik ^{[1
]}

Hofmann, Martine Catharina Josephine ^{[2
]}

Raue, Rebecca ^{[1
]}

Palmer, Gaby ^{[3
,4
]}

Brune, Bernhard ^{[1
,2
]}

de Bruin, Natasja ^{[2
]}

Weigert, Andreas ^{[1
]}

机构：

[1] Goethe Univ Frankfurt, Fac Med, Inst Biochem 1, D-60590 Frankfurt, Germany

[2] Fraunhofer Inst Translat Med & Pharmacol, D-65926 Frankfurt, Germany

[3] Univ Geneva, Dept Pathol Immunol, Sch Med, CH-1211 Geneva, Switzerland

[4] Univ Hosp, Dept Med, Div Rheumatol, CH-1211 Geneva, Switzerland

来源：

JOURNAL OF IMMUNOLOGY | 2021年 / 206卷 / 05期

关键词：

MYELIN OLIGODENDROCYTE GLYCOPROTEIN; IL-17; PRODUCTION; GAMMA-DELTA; T-CELLS; RECEPTOR; MACROPHAGES; EXPRESSION; CYTOKINE; BETA; INTERLEUKIN-38;

D O I：

10.4049/jimmunol.2000923

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：1058 / 1066

页数：9

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