دورية أكاديمية

Nicotinic attenuation of central nervous system inflammation and autoimmunity.

التفاصيل البيبلوغرافية
العنوان: Nicotinic attenuation of central nervous system inflammation and autoimmunity.
المؤلفون: Shi FD; Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013, USA. Fu-Dong.Shi@chw.edu, Piao WH, Kuo YP, Campagnolo DI, Vollmer TL, Lukas RJ
المصدر: Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2009 Feb 01; Vol. 182 (3), pp. 1730-9.
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 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: Anti-Inflammatory Agents, Non-Steroidal/*therapeutic use , Autoimmune Diseases/*immunology , Autoimmune Diseases/*prevention & control , Encephalomyelitis, Acute Disseminated/*immunology , Encephalomyelitis, Acute Disseminated/*prevention & control , Immunosuppressive Agents/*therapeutic use , Nicotine/*therapeutic use, Amino Acid Sequence ; Animals ; Autoimmune Diseases/pathology ; Cell Differentiation/drug effects ; Cell Differentiation/immunology ; Cells, Cultured ; Encephalomyelitis, Acute Disseminated/pathology ; Female ; Glycoproteins/toxicity ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myelin Proteolipid Protein/toxicity ; Myelin-Oligodendrocyte Glycoprotein ; Peptide Fragments/toxicity ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology
مستخلص: The expression of nicotinic acetylcholine receptors by neurons, microglia, and astrocytes suggests possibly diverse mechanisms by which natural nicotinic cholinergic signaling and exposure to nicotine could modulate immune responses within the CNS. In this study, we show that nicotine exposure significantly delays and attenuates inflammatory and autoimmune responses to myelin Ags in the mouse experimental autoimmune encephalomyelitis model. In the periphery, nicotine exposure inhibits the proliferation of autoreactive T cells and alters the cytokine profile of helper T cells. In the CNS, nicotine exposure selectively reduces numbers of CD11c(+) dendritic and CD11b(+) infiltrating monocytes and resident microglial cells and down-regulates the expression of MHC class II, CD80, and CD86 molecules on these cells. The results underscore roles of nicotinic acetylcholine receptors and nicotinic cholinergic signaling in inflammatory and immune responses and suggest novel therapeutic options for the treatment of inflammatory and autoimmune disorders, including those that affect the CNS.
معلومات مُعتمدة: R01 AI052463 United States AI NIAID NIH HHS
المشرفين على المادة: 0 (Anti-Inflammatory Agents, Non-Steroidal)
0 (Glycoproteins)
0 (Immunosuppressive Agents)
0 (Myelin Proteolipid Protein)
0 (Myelin-Oligodendrocyte Glycoprotein)
0 (Peptide Fragments)
0 (myelin oligodendrocyte glycoprotein (35-55))
0 (myelin proteolipid protein (139-151))
6M3C89ZY6R (Nicotine)
تواريخ الأحداث: Date Created: 20090122 Date Completed: 20090330 Latest Revision: 20190516
رمز التحديث: 20221213
DOI: 10.4049/jimmunol.182.3.1730
PMID: 19155522
قاعدة البيانات: MEDLINE
الوصف
تدمد:1550-6606
DOI:10.4049/jimmunol.182.3.1730