Peripheral Blood CD8+ T Cells CCR5 Expression and Its Δ32 Mutation in Iranian Patients with Occult Hepatitis B Infections

被引:13
作者
Arababadi, Mohammad Kazemi [1 ]
Pourfathollah, Ali Akbar [2 ]
Jafarzadeh, Abdollah [1 ]
Hassanshahi, Gholamhossein [1 ]
Mohit, Maryam [3 ]
Hajghani, Masomeh [3 ]
Shamsizadeh, Ali [4 ]
机构
[1] Rafsanjan Univ Med Sci, Fac Med, Dept Microbiol Hematol & Immunol, Rafsanjan, Iran
[2] Tarbiat Modares Univ, Sch Med Sci, Dept Immunol, Tehran, Iran
[3] Kerman Univ Med Sci, Kerman Bahonar Hosp, Dept Pathol, Kerman, Iran
[4] Rafsanjan Univ Med Sci, Fac Med, Dept Physiol, Rafsanjan, Iran
来源
LABMEDICINE | 2010年 / 41卷 / 04期
关键词
Occult hepatitis B infection; CCR5; CD8(+) T cells; HBsAg; HBV-DNA; Delta; 32; mutation; IMMUNE-RESPONSES; LIVER; POLYMORPHISMS; INVOLVEMENT; LYMPHOCYTES; HBV;
D O I
10.1309/LMVUKWROX0EBQR01
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Background: The main purpose of this study was to investigate the expression of the CCR5 and the Delta 32 mutation in its gene on the CD8(+) T cells in blood donors suffering from an occult hepatitis B infection (OBI). Methodology: The studied population included 57 OBI HBsAg/anti-HBc(+) patients with positive HBV-DNA. Flow cytometric analysis and Gap-PCR was performed to examine the expression of CCR5 on CD8(+) T cells and CCR5-Delta 32 mutations, respectively. Results: Flow cytometric analysis indicated that the number of cells which simultaneously co-express CD8 and CCR5 are decreased significantly in patients; no OBI patients had CCR5-432 mutations. Conclusions: Based on the results of this study, it can be concluded that the expression of CCR5 on CD8(+) T cells is defected in OBI patients. This may be directly related to the CCR5 gene defect (primary abnormality) or CCR5 expressing inducers (secondary abnormality), such as cytokines.
引用
收藏
页码:226 / 230
页数:5
相关论文
共 20 条
[1]   CCR5 in T cell-mediated liver diseases: What's going on? [J].
Ajuebor, Maureen N. ;
Carey, Jillian A. ;
Swain, Mark G. .
JOURNAL OF IMMUNOLOGY, 2006, 177 (04) :2039-2045
[2]   A novel CCR5/CXCR3 antagonist protects intestinal ischemia/reperfusion injury [J].
Akahori, T. ;
Sho, M. ;
Kashizuka, H. ;
Nomi, T. ;
Kanehiro, H. ;
Nakajima, Y. .
TRANSPLANTATION PROCEEDINGS, 2006, 38 (10) :3366-3368
[3]  
Arababadi MK, 2009, SAUDI J KIDNEY DIS T, V20, P398
[4]  
Arababadi Mohammad Kazemi, 2008, Pak J Biol Sci, V11, P1738, DOI 10.3923/pjbs.2008.1738.1741
[5]   Involvement of CCR5 in the passage of Th1-type cells across the blood-retina barrier in experimental autoimmune uveitis [J].
Crane, Isabel J. ;
Xu, Heping ;
Wallace, Carol ;
Manivannan, Ayyakkannu ;
Mack, Matthias ;
Liversidge, Janet ;
Marquez, Gabriel ;
Sharp, Peter F. ;
Forrester, John V. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2006, 79 (03) :435-443
[6]   Early kinetics of innate and adaptive immune responses during hepatitis B virus infection [J].
Fisicaro, P. ;
Valdatta, C. ;
Boni, C. ;
Massari, M. ;
Mori, C. ;
Zerbini, A. ;
Orlandini, A. ;
Sacchelli, L. ;
Missale, G. ;
Ferrari, C. .
GUT, 2009, 58 (07) :974-982
[7]   Analysis of CCR5, CCR2, SDF1 and RANTES gene polymorphisms in subjects with HIV-related PML and not determine leukoencephalopathy [J].
Guerini, Franca R. ;
Delbue, Serena ;
Zanzottera, Milena ;
Agliardi, Cristina ;
Saresella, Marina ;
Mancuso, Roberta ;
Maserati, Renato ;
Marchioni, Enrico ;
Gori, Andrea ;
Ferrante, Pasquale .
BIOMEDICINE & PHARMACOTHERAPY, 2008, 62 (01) :26-30
[8]   Immune responses during acute and chronic infection with hepatitis C virus [J].
Ishii, Shigeaki ;
Koziel, Margaret James .
CLINICAL IMMUNOLOGY, 2008, 128 (02) :133-147
[9]  
Jafarzadeh A., 2008, Acta Medica Iranica, V46, P27
[10]   CCR5Δ32 59537-G/A promoter polymorphism is associated with low translational efficiency and the loss of CCR5Δ32 protective effects [J].
Jin, Qingwen ;
Agrawal, Lokesh ;
Meyer, L. ;
Tubiana, R. ;
Theodorou, Ioannis ;
Alkhatib, Ghalib .
JOURNAL OF VIROLOGY, 2008, 82 (05) :2418-2426