TY - JOUR
T1 - New insights into the role of IL-1b in experimental autoimmune encephalomyelitis and multiple sclerosis
AU - Lin, Chih Chung
AU - Edelson, Brian T.
N1 - Funding Information:
This work was supported by National Institutes of Health Grant R01 AI113118 (to B.T.E.), a Burroughs Wellcome Fund Career Award for Medical Scientists (to B.T.E.), and the McDonnell International Scholars Academy at Washington University (to C.-C.L.).
Publisher Copyright:
Copyright © 2017 by The American Association of Immunologists, Inc.
PY - 2017/6/15
Y1 - 2017/6/15
N2 - Multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells that elicit demyelination and axonal damage. How TH cells acquire pathogenicity and communicate with myeloid cells and cells of the CNS remain unclear. IL-1β is recognized to play an important role in experimental autoimmune encephalomyelitis (EAE) and perhaps MS. Clinical EAE is significantly attenuated in IL-1R-deficient and IL-1β-deficient mice, and IL-1β is found in the blood, cerebrospinal fluid, and CNS lesions of MS patients. In this article, we focus on new reports that elucidate the cellular sources of IL-1β and its actions during EAE, in both lymphoid tissues and within the CNS. Several immune cell types serve as critical producers of IL-1β during EAE, with this cytokine inducing response in both hematopoietic and nonhematopoietic cells. These findings from the EAE model should inspire efforts toward investigating the therapeutic potential of IL-1 blockade in MS.
AB - Multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis, are neuroinflammatory diseases driven by autoreactive pathogenic TH cells that elicit demyelination and axonal damage. How TH cells acquire pathogenicity and communicate with myeloid cells and cells of the CNS remain unclear. IL-1β is recognized to play an important role in experimental autoimmune encephalomyelitis (EAE) and perhaps MS. Clinical EAE is significantly attenuated in IL-1R-deficient and IL-1β-deficient mice, and IL-1β is found in the blood, cerebrospinal fluid, and CNS lesions of MS patients. In this article, we focus on new reports that elucidate the cellular sources of IL-1β and its actions during EAE, in both lymphoid tissues and within the CNS. Several immune cell types serve as critical producers of IL-1β during EAE, with this cytokine inducing response in both hematopoietic and nonhematopoietic cells. These findings from the EAE model should inspire efforts toward investigating the therapeutic potential of IL-1 blockade in MS.
UR - http://www.scopus.com/inward/record.url?scp=85020428204&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1700263
DO - 10.4049/jimmunol.1700263
M3 - Review article
C2 - 28583987
AN - SCOPUS:85020428204
SN - 0022-1767
VL - 198
SP - 4553
EP - 4560
JO - Journal of Immunology
JF - Journal of Immunology
IS - 12
ER -