Evaluation of CCR5 expression on NK cells in Iranian patients with occult hepatitis B infection
Author(s)
Arababadi, Mohammad Kazemi
Pourfathollah, Ali Akbar
Jafarzadeh, Abdollah
Hassanshahi, Gholamhossein
Mohit, Maryam
Hajghani, Masomeh
Ahmadabadi, Behzad Nasiri
Kennedy, Derek
Griffith University Author(s)
Year published
2010
Metadata
Show full item recordAbstract
Background: Chemotactic cytokine (CC) motif receptor type 5 (CCR5) also known as "cluster of differentiation 195" (CD195), is found on the surface of natural killer (NK) cells which play a critical role in host antiviral defense. NK cells are involved in immunity against overt and occult hepatitis B virus (HBV) infection. Occult HBV infection (OBI) is characterized by the presence of HBV-DNA despite the absence of hepatitis B surface antigen (HBsAg) in the serum of infected patients. The CCR5 receptor and its ligands play an important role in the immune defense mechanism against HBV. Material and methods: We tested 3700 ...
View more >Background: Chemotactic cytokine (CC) motif receptor type 5 (CCR5) also known as "cluster of differentiation 195" (CD195), is found on the surface of natural killer (NK) cells which play a critical role in host antiviral defense. NK cells are involved in immunity against overt and occult hepatitis B virus (HBV) infection. Occult HBV infection (OBI) is characterized by the presence of HBV-DNA despite the absence of hepatitis B surface antigen (HBsAg) in the serum of infected patients. The CCR5 receptor and its ligands play an important role in the immune defense mechanism against HBV. Material and methods: We tested 3700 plasma samples for the presence of HBsAg, hepatitis B core antibody (anti-HBc), and HBV-DNA to identify patients who were HBsAg negative, anti-HBc positive, and HBV-DNA positive (HBsAg-/anti-HBc+/HBV-DNA+) and considered as OBI. Subsequently CD195/CCR5 was used a marker in flow cytometry to isolate NK cells from OBI patients. Results: From the original pool of 3700 patients 352 (9.5%) plasma samples were HBsAg-/anti-HBc+. Among these samples, 57 were HBV-DNA+, representing a total of 57 OBI patients. Flow cytometric analysis indicated that the number and intensity of CCR5/CD195+ NK cells was decreased in cell samples from all of our OBI patients. Conclusion: NK cells in OBI patients may be unable to express sufficient CCR5 to mount an effective immune response to HBV infection.
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View more >Background: Chemotactic cytokine (CC) motif receptor type 5 (CCR5) also known as "cluster of differentiation 195" (CD195), is found on the surface of natural killer (NK) cells which play a critical role in host antiviral defense. NK cells are involved in immunity against overt and occult hepatitis B virus (HBV) infection. Occult HBV infection (OBI) is characterized by the presence of HBV-DNA despite the absence of hepatitis B surface antigen (HBsAg) in the serum of infected patients. The CCR5 receptor and its ligands play an important role in the immune defense mechanism against HBV. Material and methods: We tested 3700 plasma samples for the presence of HBsAg, hepatitis B core antibody (anti-HBc), and HBV-DNA to identify patients who were HBsAg negative, anti-HBc positive, and HBV-DNA positive (HBsAg-/anti-HBc+/HBV-DNA+) and considered as OBI. Subsequently CD195/CCR5 was used a marker in flow cytometry to isolate NK cells from OBI patients. Results: From the original pool of 3700 patients 352 (9.5%) plasma samples were HBsAg-/anti-HBc+. Among these samples, 57 were HBV-DNA+, representing a total of 57 OBI patients. Flow cytometric analysis indicated that the number and intensity of CCR5/CD195+ NK cells was decreased in cell samples from all of our OBI patients. Conclusion: NK cells in OBI patients may be unable to express sufficient CCR5 to mount an effective immune response to HBV infection.
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Journal Title
Laboratory Medicine
Volume
41
Issue
12
Copyright Statement
Self-archiving of the author-manuscript version is not yet supported by this journal. Please refer to the journal link for access to the definitive, published version or contact the authors for more information.
Subject
Medical genetics (excl. cancer genetics)