Research Article Open Access Kady et al., J Clin Cell Immunol 2017, 8:3 DOI: 10.4172/2155-9899.1000504 Research Article OMICS International Journal of Clinical & Cellular Immunology J o u r n a l o f C l i n i c a l & C e ll u l a r I m m u n o l o g y ISSN: 2155-9899 Volume 8 • Issue 3 • 1000504 J Clin Cell Immunol, an open access journal ISSN: 2155-9899 *Corresponding author: Marwa Abd El Azim Mansour, Associate Professor of Medical Microbiology and Immunology, Faculty of Medicine, Zagazig University, Egypt, E-mail: marwa_abdelazimm@yahoo.com Received: March 29, 2017; Accepted: May 09, 2017; Published: May 22, 2017 Citation: Kady LMA, Mansour MA, Gobran ST, Ahmad EI (2017) Natural Killer Cell Subsets Distribution in Spontaneously Resolved and Chronic Persistent Hepatitis C Virus Infection. J Clin Cell Immunol 8: 504. doi: 10.4172/2155-9899.1000504 Copyright: © 2017 Kady LMA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Natural Killer Cell Subsets Distribution in Spontaneously Resolved and Chronic Persistent Hepatitis C Virus Infection Laila M Al Kady 1 , Marwa A Mansour 1 *, Samaa T Gobran 1 and Ebtesam I Ahmad 2 1 Medical Microbiology and Immunology Department, Faculty of Medicine, Zagazig University, Egypt 2 Clinical Pathology, Faculty of Medicine, Zagazig University, Egypt Keywords: Global Fund’s support; HIV/AIDS; hailand; Transition Introduction Hepatitis C virus (HCV) infection is one of the main causes of chronic liver disease worldwide. he long-term impact of chronic persistent HCV infection is highly variable, ranging from minimal histological changes to extensive ibrosis and cirrhosis with or without hepatocellular carcinoma [1]. Natural killer (NK) cells are large granular lymphocytes that account for the majority of innate immune cells in the human liver. hey play an important role in the control of viral infections. heir functions are mediated by a diverse array of inhibitory and activating cell-surface receptors [2]. In human peripheral blood, the CD3-NK cells are divided into ive subpopulations which can be deined on the basis of the relative expression of the markers CD16 (Fc γ RIII) and CD56:CD56 dim CD16 + , CD56 dim CD16-, CD56 bright CD16 − , CD56 bright CD16 + , and CD56 − CD16 + [3]. CD56 +dim CD16 + NK cells normally account approximately 90% of peripheral NK cells. hey usually express CD16 which is the Fc receptor for IgG, killer cell immunoglobulin-like receptors (KIRs) and homing markers for inlamed peripheral sites. hey carry perforin, and are the main mediators of NK cytotoxicity [4]. CD56 +bright CD16 − NK cells account nearly 10% of peripheral NK cells. hey express homing markers for secondary lymphoid tissues where they accumulate. hey do not express KIRs, contain low levels of perforin, and are only weakly cytotoxic. However, they are important secretors of cytokines including IFN-gamma, TNF-α, granulocyte- macrophage colony-stimulating factor (GMCSF), interleukin 10 (IL10) and IL13 [5]. Most prominent among NK receptors are the killer cell immunoglobulin-like receptors (KIRs). CD158b is one of KIRs which confers inhibitory signals to NK cells leading to their suppression [6]. In chronic persistent HCV infection, NK cells display alterations in their phenotype and function, and cytolytic NK cells seem to be impaired through high expression of inhibitory receptors including CD 158b [7]. On the other hand, CD158b low frequency seems to predict resolution of chronic persistent HCV infection. Also, CD158b may correlate with some diagnostic parameters in chronic HCV patients [8]. On contrary, in spontaneously resolved HCV infection, the activated NK cells' responses suggest an important contribution to resolution of the infection, as there is a good cytolytic function of NK cell and normal expression of inhibitory cell surface receptors [9]. Material and Methods he aim of this work was to study the frequency of the NK cell and the distribution of its subsets in spontaneously resolved and chronic persistent hepatitis C virus infection. In addition, to study the frequency of inhibitory receptor CD158b in these clinical outcomes and to correlate its frequency with certain clinical and diagnostic parameters. Abstract Altered frequency and distribution of natural killer cell subsets have been reported in hepatitis C virus (HCV) infection.We investigated the frequency of NK cells and inhibitory receptor CD158 in a sample of Egyptian patients with spontaneously resolved (SR) and chronic persistent hepatitis C virus (CPHC) infection, and correlated data with other clinical and diagnostic parameters. The study was conducted on 48 patients divided into 3 groups. Group I; 16 CPHC patients, Group II; 16 SR individuals and Group III; 16 healthy controls. Chronic persistent HCV patients and SR individual’s data were reported from patients ' reports. Healthy controls serum antibodies against HCV were measured using ELISA technique. The three studied groups fresh peripheral blood samples were analyzed by low cytometry to determine total NK cells, their subsets and CD158b + cells percentages. Total NK cells and CD56 +dim CD16 + NK cells were signiicantly decreased in CPHC patients and SR individuals in comparison to healthy controls(P<0.001).In contrast, CD56 +bright CD16 − NK cells were signiicantly increased in CPHC patients and reduced in SR individuals in comparison with healthy controls (P<0.001). Signiicant elevation of CD158b inhibitory receptor frequency in CPHC patients in comparison with healthy controls (P<0.001) and it was positively correlated with stage of cirrhosis, unresponsiveness to IFN, WBCs and lymphocytes counts and AST and ALT levels. In conclusion, during the chronic HCV infection stage, the frequency of NK cells is signiicantly depressed and CD158b+ inhibitory receptor might be represent this impairment. On the other hand, in SR individuals, total NK cells were signiicantly decreased. Also, CD56 +dim CD16 + NK cells and CD56 +bright CD16− NK cells percentages were signiicantly decreased (P<0.001) although preserving nearly the same ratio of healthy controls. Also, there was no signiicant elevation in CD158b + cells frequency (P>0.05).