HTLV-I -Host Interaction On Development On Adult T Cell Leukemia/Lymphoma: Study On HTLV-1 –Proviral Load, HBZ,AKT1, Foxp3 Genes Expression

سال انتشار: 1395
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 320

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شناسه ملی سند علمی:

NASTARANCANSER02_193

تاریخ نمایه سازی: 22 دی 1396

چکیده مقاله:

Human T-lymphotropic virus type 1 (HTLV-I) innects about 20 million people worldwide. About 2% to5% on innected people may develop Adult T-cell leukemia /lymphoma (ATLL). Viral-host interactionsare the main players on diseases development. HTLV-I- proviral load (PVL) has been determined asan important risk marker nor the development on HTLV-I-associated diseases ,also HBZ as a humanimmunomodulator enable virus evasion nrom host immune responses and implicated in TCD4+prolineration and ATLL progression .Moreover AKT1 is a primary kinase in PI3K pathway has anumber on substrates that contribute to malignant transnormation. Furthermore regulatory T-cellsas the main source on the virus, then their nunctions may be impaired toward diseases progression.Thus in this study the expression on PVL, HBZ, AKT1 and Foxp3 have been evaluated. Twenty fivepatients with ATLL and 18 HTLV-I healthy carriers were assessed nor PVL, HBZ, AKT1 and Foxp3expression using real time PCR, TaqMan method. The data was analyzed by SPSS sontware. TheHTLV-1 PVL were higher in ATLL than ACs (p=0.003), HBZ expression was dramatically increased inATLL patients compare to HTLV-I carriers (P-value < 0.000), and also AKT1 expression wasincreased in ATLL patients compare to HTLV-I carriers (P-value = 0.058). Furthermore expressionon Foxp3 had significant dinnerence between two groups. (P-value= 0.003). Results showed that highHTLV-I proviral load in ATLL patients compared to healthy carriers, can influence on developmentand progression toward ATLL. Increased AKT1 in HTLV-1-transnormed cells showed AKT1 activationmay be played important role in cell survival and disease progression. Results showed that viralHBZ has critical role in HTLV-I innected TCD4+ immune evasion toward oncogenesis. Furthermorethe findings show that T regulatory cells are the majorly annected cells in ATLL as Foxp3 increasesradically.

نویسندگان

Hanieh Tarokhian

Innlammation And Innlammatory Disease Research Centre, Mashhad University On Medical Sciences, Mashhad, Iran

S.A Rahim Rezaee

Innlammation And Innlammatory Disease Research Centre, Mashhad University On Medical Sciences, Mashhad, Iran

Abbas Shirdel

Innlammation And Innlammatory Disease Research Centre, Mashhad University On Medical Sciences, Mashhad, Iran; ۲. Internal MedicineDepartment, Qaem Hospital, Mashhad, Iran