کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10803606 | 1057162 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TLR mediated GSK3β activation suppresses CREB mediated IL-10 production to induce a protective immune response against murine visceral leishmaniasis
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کلمات کلیدی
CREBGSKLPSTLRPAMPiNOSb.w.pathogen-associated molecular patterns - الگوهای مولکولی مرتبط با پاتوژنCSA - ایالات مؤتلفهٔ آمریکاinterleukin - اینترلوکینToll-like receptor - تیالآرinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییnuclear extract - عصاره هسته ایLeishmania donovani - لیشمانیا دونووانیVisceral leishmaniasis - لیشمانیاز احشایی، کالاآزارlipopolysaccharide - لیپوپلی ساکاریدNitric oxide - نیتریک اکسیدbody weight - وزن بدنcAMP response element-binding protein - پروتئین واکنش القا کننده واکنش cAMPglycogen synthase kinase 3 - گلیکوزین سنتاز کیناز 3glycogen synthase kinase - گلیکوزین سیتستاز کیناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: TLR mediated GSK3β activation suppresses CREB mediated IL-10 production to induce a protective immune response against murine visceral leishmaniasis TLR mediated GSK3β activation suppresses CREB mediated IL-10 production to induce a protective immune response against murine visceral leishmaniasis](/preview/png/10803606.png)
چکیده انگلیسی
During Leishmania donovani (LD) infection Interleukin (IL)-10 favors parasite replication and plays a central role as a target for immune-based therapy. Glycogen synthase kinase 3 (GSK3)β differentially regulates TLR-mediated cytokine production. CREB, an important transcription factor that induces IL-10 production is negatively regulated by GSK3β. However, down regulation of IL-10 via CREB suppression has not been well explored in controlling LD infection. Here we demonstrate that, the TLR4 agonist 29 KDa β 1,4-galactose terminal glycoprotein (GP29) of LD activated GSK3β through TLR4 to induce IL-12-mediated Nitric oxide (NO) production that resulted in effective parasite clearance from macrophages. GSK3β activation abrogated both CREB phosphorylation and IL-10 production. Two subcutaneous injections of GP29 at fortnightly intervals in a 4-week infected mouse model of LD resulted in a dominant IL-12-mediated NO production and 100% animals were protected against a subsequent challenge with virulent LD parasites. Complete absence of GP29 mediated protection with down regulated NO and IL-12 production and dominant IL-10 production in presence of the GSK3β inhibitor, Lithium chloride reiterated the role of GSK3β in disease resolution in the murine model of visceral leishmaniasis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimie - Volume 107, Part B, December 2014, Pages 235-246
Journal: Biochimie - Volume 107, Part B, December 2014, Pages 235-246
نویسندگان
Joydeep Paul, Kshudiram Naskar, Sayan Chowdhury, Tapati Chakraborti, Tripti De,