دورية أكاديمية

GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but Is Dispensable for Disease Induction.

التفاصيل البيبلوغرافية
العنوان: GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but Is Dispensable for Disease Induction.
المؤلفون: Duncker PC; Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Multiple Sclerosis Center, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Graduate Program in Immunology, University of Michigan School of Medicine, Ann Arbor, MI 48109; and., Stoolman JS; Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Multiple Sclerosis Center, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Graduate Program in Immunology, University of Michigan School of Medicine, Ann Arbor, MI 48109; and., Huber AK; Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Multiple Sclerosis Center, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109., Segal BM; Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109; bmsegal@med.umich.edu.; Multiple Sclerosis Center, Department of Neurology, University of Michigan School of Medicine, Ann Arbor, MI 48109.; Graduate Program in Immunology, University of Michigan School of Medicine, Ann Arbor, MI 48109; and.; Neuroscience Program, University of Michigan School of Medicine, Ann Arbor, MI 48109.
المصدر: Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2018 Feb 01; Vol. 200 (3), pp. 966-973. Date of Electronic Publication: 2017 Dec 29.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1550-6606 (Electronic) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE
أسماء مطبوعة: Publication: Bethesda, MD : American Association of Immunologists
Original Publication: Baltimore : Williams & Wilkins, c1950-
مواضيع طبية MeSH: CD4-Positive T-Lymphocytes/*immunology , Central Nervous System/*cytology , Central Nervous System/*pathology , Encephalomyelitis, Autoimmune, Experimental/*pathology , Granulocyte-Macrophage Colony-Stimulating Factor/*immunology , Myelin-Oligodendrocyte Glycoprotein/*immunology, Adoptive Transfer ; Animals ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/transplantation ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Lung/pathology ; Lymph Nodes/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelin-Oligodendrocyte Glycoprotein/administration & dosage ; Neutrophils/immunology ; Peptide Fragments/administration & dosage ; Peptide Fragments/immunology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
مستخلص: GM-CSF has been portrayed as a critical cytokine in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and, ostensibly, in multiple sclerosis. C57BL/6 mice deficient in GM-CSF are resistant to EAE induced by immunization with myelin oligodendrocyte glycoprotein (MOG) 35-55 The mechanism of action of GM-CSF in EAE is poorly understood. In this study, we show that GM-CSF augments the accumulation of MOG 35-55 -specific T cells in the skin draining lymph nodes of primed mice, but it is not required for the development of encephalitogenic T cells. Abrogation of GM-CSF receptor signaling in adoptive transfer recipients of MOG 35-55 -specific T cells did not alter the incidence of EAE or the trajectory of its initial clinical course, but it limited the extent of chronic CNS tissue damage and neurologic disability. The attenuated clinical course was associated with a relative dearth of MOG 35-55 -specific T cells, myeloid dendritic cells, and neutrophils, as well as an abundance of B cells, within CNS infiltrates. Our data indicate that GM-CSF drives chronic tissue damage and disability in EAE via pleiotropic pathways, but it is dispensable during early lesion formation and the onset of neurologic deficits.
(Copyright © 2018 by The American Association of Immunologists, Inc.)
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معلومات مُعتمدة: R01 NS105385 United States NS NINDS NIH HHS; R21 NS103215 United States NS NINDS NIH HHS; T32 AI007413 United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Csf2ra protein, mouse)
0 (Myelin-Oligodendrocyte Glycoprotein)
0 (Peptide Fragments)
0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor)
0 (myelin oligodendrocyte glycoprotein (35-55))
83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
تواريخ الأحداث: Date Created: 20171231 Date Completed: 20181001 Latest Revision: 20190201
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC5780231
DOI: 10.4049/jimmunol.1701484
PMID: 29288202
قاعدة البيانات: MEDLINE
الوصف
تدمد:1550-6606
DOI:10.4049/jimmunol.1701484