Prethodne studije su pokazale da leptin i rastvorljivi leptinski receptor (SLR) mogu uticati na upalne i imunske procese kod autoimunskih bolesti, ali to ostaje nejasno kod sistemskog eritemskog lupusa (SLE). Cilj istrajednog istraživanja u 2015. bio je procijena da li su leptin i SLR uključeni u etiopatologiju SLE i mogući mehanizam imunske regulacije. Proučavano je 87 pacijenata sa SLE i 85 podudarnih ispitanika.
Procijenjeni su nivoi leptina i SLR u serumu, testirani nivoi iRNK receptora duge izoforme leptina (Ob-Rb) kod pacijenata sa SLE i kontrolne grupe. Nadalje, određen je postotak Th1 i Th2 u limfocitima pacijenata sa SLE i ispitivana aktivacija i ćelijska proliferacija limfocita, uz stimulaciju leptinom in vitro. Studija je otkrila viši nivo leptina u serumu kod pacijenata sa SLE, ali nije pronađena razlika u serumskim nivoima SLR ili nivoima Ob-Rb iRNK između pacijenata sa SLE i kontrolne grupe. Procenat Th1 ćelija se smanjio, a Th2 ćelija povećao nakon tretmana glukokortikoidima kod pacijenata sa SLE. Leptin je stimulirao proliferaciju T-ćelijain vitro, a diferencijacija Th1-ćelija se povećala. Ova studija je pokazala da leptin može imati važnu ulogu u patogenezi SLE, izazivajući disfunkciju autoimunskih procesa.[3]
Reference
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Liangliang Ma, Dandan Li, Manish Rai Sookha, Meiyun Fang, Yanchun Guan, Xiangnan Sun, Jingfan Guan (2015): Elevated serum leptin levels in patients with systemic lupus erythematosus. Pharmazie, 70(11):720-723
Dopunska literatura
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