多发性硬化症是一种影响患者神经系统的自体免疫疾病，导致患者身体和认知功能的丧失。如今，研究人员鉴别出一种可能是影响进展性多发性硬化症的因子，新成果发表在8月在线出版的《自然—免疫学》期刊上。
多发性硬化症有不同类型的疾病进展模式。临床上，依病程进展可分为四类：复发—缓解型、次发—渐进型、首发—渐进型和渐进—复发型。其疾病的进展又可简单分为两个阶段，复发—缓解型阶段主要为免疫引起的发炎反应，而渐进阶段则包含了神经的退化。
但在复发—缓解型阶段后，病情会出现不可逆转的进展型发展。目前还没有针对这种进展型多发性硬化症的有效疗法。
Howard Weiner和Francisco Quintana领导的一个研究小组鉴别出一种名为15-HC的脂肪，这种脂肪在进展型患者体内的含量提高了，而在复发—缓解型患者体内却没有这种情况。科学家们发现，15-HC激活了一种名为PARP-1的受体，阻止了PARP-1的活性，降低了进展型多发性硬化症模式小鼠的病程。
进一步的研究还将确认一个新问题：控制PARP-1的活性是否治疗进展型多发性硬化症的潜在方法。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology 16 August 2009 | doi:10.1038/ni.1775
Toll-like receptor 2 and poly(ADP-ribose) polymerase 1 promote central nervous system neuroinflammation in progressive EAE
Mauricio F Farez1,4, Francisco J Quintana1,4, Roopali Gandhi1, Guillermo Izquierdo2,3, Miguel Lucas2 & Howard L Weiner1
Abstract
Multiple sclerosis is an inflammatory disease of the central nervous system that begins as a relapsing-remitting disease (RRMS) and is followed by a progressive phase (SPMS). The progressive phase causes the greatest disability and has no effective therapy, but the processes that drive SPMS are mostly unknown. Here we found higher serum concentrations of 15-hydroxicholestene (15-HC) in patients with SPMS and in mice with secondary progressive experimental autoimmune encephalomyelitis (EAE) but not in patients with RRMS. In mice, 15-HC activated microglia, macrophages and astrocytes through a pathway involving Toll-like receptor 2 (TLR2) and poly(ADP-ribose) polymerase 1 (PARP-1). PARP-1 activity was higher in monocytes of patients with SPMS, and PARP-1 inhibition suppressed the progression of EAE. Thus, the TLR2–PARP-1 pathway is a potential new therapeutic target in SPMS.
1 Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
2 Molecular Biology Service, University of Sevilla, Sevilla, Spain.
3 Multiple Sclerosis Unit, University of Sevilla, Sevilla, Spain.
4 These authors contributed equally to this work.
