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1
T cells in multiple sclerosis and experimental autoimmune encephalomyelitis.
Clin Exp Immunol. 2010 Oct;162(1):1-11. doi: 10.1111/j.1365-2249.2010.04143.x.
2
Role of Th17 cells in the pathogenesis of CNS inflammatory demyelination.
J Neurol Sci. 2013 Oct 15;333(1-2):76-87. doi: 10.1016/j.jns.2013.03.002. Epub 2013 Apr 8.
4
NLRP3 plays a critical role in the development of experimental autoimmune encephalomyelitis by mediating Th1 and Th17 responses.
J Immunol. 2010 Jul 15;185(2):974-81. doi: 10.4049/jimmunol.0904145. Epub 2010 Jun 23.
5
Emerging concepts in autoimmune encephalomyelitis beyond the CD4/T(H)1 paradigm.
Ann Anat. 2010 Aug 20;192(4):179-93. doi: 10.1016/j.aanat.2010.06.006. Epub 2010 Jul 15.
9
Th17 Cells and autoimmune encephalomyelitis (EAE/MS).
Allergol Int. 2008 Jun;57(2):115-20. doi: 10.2332/allergolint.R-07-159.
10
Lineage-Specific Metabolic Properties and Vulnerabilities of T Cells in the Demyelinating Central Nervous System.
J Immunol. 2017 Jun 15;198(12):4607-4617. doi: 10.4049/jimmunol.1600825. Epub 2017 May 15.

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Hemoglobin alpha regulates T-lymphocyte activation and mitochondrial function.
bioRxiv. 2025 Aug 2:2025.08.01.668160. doi: 10.1101/2025.08.01.668160.
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Understanding the Blood-Brain Barrier: From Physiology to Pathology.
Adv Exp Med Biol. 2025;1477:1-33. doi: 10.1007/978-3-031-89525-8_1.
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Exploring the Potential Link Between Autoimmune Diseases and Pan-Cancer: A Multidatabase Mendelian Randomization Analysis.
J Immunol Res. 2025 Apr 27;2025:6468979. doi: 10.1155/jimr/6468979. eCollection 2025.
5
Impact of High-Efficacy Therapies for Multiple Sclerosis on B Cells.
Cells. 2025 Apr 17;14(8):606. doi: 10.3390/cells14080606.
6
Experimental autoimmune encephalomyelitis pathogenesis alters along animal age: impact of S100B expression.
J Neuroimmune Pharmacol. 2025 Apr 14;20(1):37. doi: 10.1007/s11481-025-10195-5.
8
BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation.
Cell Rep. 2025 Mar 25;44(3):115393. doi: 10.1016/j.celrep.2025.115393. Epub 2025 Mar 8.
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Discovering root causal genes with high-throughput perturbations.
Elife. 2025 Mar 5;13:RP100949. doi: 10.7554/eLife.100949.

本文引用的文献

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CD39+Foxp3+ regulatory T Cells suppress pathogenic Th17 cells and are impaired in multiple sclerosis.
J Immunol. 2009 Dec 1;183(11):7602-10. doi: 10.4049/jimmunol.0901881. Epub 2009 Nov 16.
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Transforming growth factor beta is dispensable for the molecular orchestration of Th17 cell differentiation.
J Exp Med. 2009 Oct 26;206(11):2407-16. doi: 10.1084/jem.20082286. Epub 2009 Sep 28.
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IL-17 as a future therapeutic target for rheumatoid arthritis.
Nat Rev Rheumatol. 2009 Oct;5(10):549-53. doi: 10.1038/nrrheum.2009.179.
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Psoriasis market.
Nat Rev Drug Discov. 2009 Oct;8(10):767-8. doi: 10.1038/nrd2996.
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Novel CD8+ Treg suppress EAE by TGF-beta- and IFN-gamma-dependent mechanisms.
Eur J Immunol. 2009 Dec;39(12):3423-35. doi: 10.1002/eji.200939441.
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Pathogenic CD8(+) T cells in multiple sclerosis.
Ann Neurol. 2009 Aug;66(2):132-41. doi: 10.1002/ana.21744.
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Encephalitogenic T cells that stably express both T-bet and ROR gamma t consistently produce IFNgamma but have a spectrum of IL-17 profiles.
J Neuroimmunol. 2009 Oct 30;215(1-2):10-24. doi: 10.1016/j.jneuroim.2009.07.007. Epub 2009 Aug 18.
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Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.
Immunity. 2009 Aug 21;31(2):331-41. doi: 10.1016/j.immuni.2009.08.001. Epub 2009 Aug 13.

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