الفهرس 
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Abstract
Hepatitis C virus (HCV) is a member of the Hepacivirus genus in the Flaviviridea family (Alter et al., 1999). Hepatocytes are the major target cells for HCV. It has been suggested that approximately less than 10% of hepatocytes become infected with HCV.
The T cell immunoglobulin mucin (Tim) family (also known as the TIM family) of cell-surface receptors regulates Th1- and Th2-mediated immunity and is implicated in a wide range of autoimmune and allergic diseases, including asthma and rheumatoid arthritis (Meyers et al., 2005b).
TIM-3 was initially cloned as a Th1-specific cell-surface marker and represents the first Tim family member implicated in immune regulation (Monney et al., 2002). Administration of TIM-3 antibody during the course of EAE augments the disease, resulting in increased mortality and an atypical hyperacute EAE (Monney et al., 2002). Subsequent studies have demonstrated that TIM-3 inhibits Th1-mediated immunity and promotes peripheral tolerance (Sabatos et al., 2003; Sanchez-Fueyo et al., 2003).
The role of TIM-3 in chronic viral infections was first identified in HCV infection. In HIV-infected patients, the frequency of TIM-3＋CD8 T cells increased, and the TIM-3 levels on the T cells correlated positively with the viral titer and inversely with CD4 T cell count. The HCV-specific CD8 T cells that overexpress Tim 3 were found to be functionally impaired, and a blockade of TIM-3 restored the functions of HCV-specific CD8 T cells (Jones et al., 2008 and Fourcade et al., 2010).
Analysis of both peripheral and intra-hepatic T-cells in individuals chronically infected with HCV, has demonstrated an increase in the frequency of TIM-3-expressing CD4+ and CD8+ T-cells in comparison to uninfected controls.
This study included 90 cases, Patients will be divided into two groups: Group 1 (35 patients) will include anti-HCV antibody positive/ HCV PCR positive patients with normal liver functions, Group 2 (35 patients) will comprise anti-HCV positive/HCV HCV PCR positive patients with abnormal liver functions, and Group 3 will involve 20 normal controls (anti-HCV antibody negative persons).
In our results, comparing the control, compensated and decompensated groups regarding lymphocytic counts, percentages of TIM3 positive cells within CD4, CD8, CD14 and CD56 cells in the three groups showed that the absolute numbers of lymphocytes and the percentage of lymphocytes was maximum in the control group, followed by the compensated group and minimum in the decompensated group, with a significant p value.
Also, the percentage of CD4 cells was higher in the compensated and control groups, than in the decompensated group, with non significant difference.
CD8-TIM3 positive cells were maximum in the decompensated groups and minimum in the control group, with a significant p value.
CD14 cells were maximum in the compensated group, followed by decompensated and minimum in the control group, again with a significant difference.
Summary and Conclusion 212
CD56 cells showed non significant differences between the three groups. There was also shows a steady increase in the percentage of Tim+ve CD4, CD8, CD14 and CD56 cells, with maximum percentages among the decompensated liver disease group, and least percentage among the control group.
Regarding vitamin D in our study, however, we found that the level of vitamin D was maximum in the control group and minimum among the decompensated group. The difference is, again, highly significant.
Conclusion
In summary, our findings demonstrate that accumulation of TIM-3+ T cells (CD4+ve,CD8+ve),CD56+ve and CD14+ve cells is associated with functional impairment, and consequently with development of persistent HCV. The present study provides a basis for improving current therapies by simultaneous blockade of multiple inhibitory pathways that could result in additive efficacy without excessive toxicity.
We also can conclude that vitamin D might play a role in HCV chronicity and can be a contributing factor in treatment of the disease.