Uloga azot-monoksida u regulaciji ekspresije CXCL12 u eksperimentalnom autoimunskom encefalomijelitisu u pacova
The role of nitric-oxide in CXCL12 expression regulation in experimental autoimmune encephalomyelitis in rats
2014
Authors:
Petković, FilipContributors
Kataranovski, MilenaMiljković, Đorđe
Mostarica-Stojković, Marija
Document Type:
Doctoral thesis (Published version)
Metadata
Show full item recordAbstract:
Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating and degenerativedisease of the central nervous system (CNS) that occurs preferentially in young adults.Immune system plays a key role in its pathogenesis. It is considered that MS develops dueto an autoimmune response directed against myelin sheet components. MS is a veryheterogeneous disease in its clinical manifestations, which is most probably a consequenceof diverse molecular mechanisms involved in its pathogenesis. As a consequence of myelinsheet destruction and axonal degeneration, transient or permanent deficits in motor, sensoryand cognitive functions appear in MS patients. Therapies which are currently in usedecrease the frequency and the severity of acute attacks and slow down the rate ofneurological deterioration, but do not cure the patients.Experimental autoimmune encephalomyelitis (EAE) is the most widely usedexperimental model for studying pathophysiology of MS. The use of this model, whichmimics autoimmune pathogenesis of MS, led to many discoveries aboutneuroimmunological processes, such as egression of immune cells from the blood streaminto the CNS, immune cell interaction with resident glial cells and neurons and subsequentinflammation, as an important aspect of MS.Chemokines are cytokines with a central role in regulation of immune cell migrationat the site of inflammation during pathogen invasion and during pathological immuneprocesses, such as MS. Most often, chemokines boost immune response by attractingimmune cells at the effector sites. However, some chemokines, including CXCL12, exertregulatory or antiinflammatory roles. CXCL12 prevents egress of autoreactive immunecells from the perivascular space into the CNS parenchyma, induces autoreactive T cellapoptosis and stimulates shifting of proinflammatory phenotype of these cells towardsantiinflammatory phenotype...
Keywords:
Multiple sclerosis; Experimental autoimmune encephalomyelitis; Nitric-oxide; CXCL12; Neuroinflammation; AstrocytesSource:
University of Belgrade, Faculty of Biology, 2014, 1-85URI
http://eteze.bg.ac.rs/application/showtheses?thesesId=3056https://fedorabg.bg.ac.rs/fedora/get/o:11306/bdef:Content/download
http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024726450
http://nardus.mpn.gov.rs/123456789/5670
https://radar.ibiss.bg.ac.rs/handle/123456789/2405