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Abstract HCV represents a global health problem affecting a high range of population worldwide. It is the main cause of liver inflammation. Meanwhile, hepatitis may be caused by an autoimmune disorder, in which the body’s immune system attacks the normal liver cells because it became unable to differentiate between harmful invaders and healthy liver tissues. Thus, differentiation between different causes of liver inflammation due to various etiologies still represents big challenge. Therefore, this study sought to develop new immunodiagnostic markers able to differentiate between different types of inflammation. The study was performed on eighty-one blood samples collected from the medical unit at the national research center starting from October 2016 till May 2019. The samples were divided into seven groups as follow: group (1); normal: nine healthy control volunteers with no history of HCV-infection, liver disturbance diseases or autoimmune diseases. group (2); HCV: eleven- HCV infected patients with no history of autoimmune diseases. group (3); HCV+auto: eleven-HCV infected patients who are positive for autoimmune markers. Summary 98 group (4); NAFL: four HCV\HBV non infected patients but had liver disturbance as nonalcoholic fatty liver. group (5); NAFL+auto: six HCV\HBV non infected patients but had liver disturbance as NAFL and are positive of autoimmune marker. group (6); RA: nineteen patients suffering from RA. group (7); SLE: twenty-one SLE patients. The levels of ALT, AST in sera, BAFF, TNF α and IL-10 were measured in plasma while the levels of TLR3, TLR7 were quantified in lysates of PBMNCs at protein levels and the relative expression of TLR3, TLR7, TNF; IL-10 in cell lysates was assessed against GAPDH by qRT-PCR from all groups. The current study demonstrated the detection of Auto-Abs, such as ANA and ASMA in patients with NAFL and HCV and their presence leads to concerns about AIH. Additionally, HCV-Ab titer can well differentiate between HCV and non-HCV infected patients, with inability to predict the progression of HCV infection to AIH. Additionally, a positive correlation between the presence of Auto-Abs and the increase in BAFF levels was also recorded in HCV and NAFL patients. At both transcriptional and protein levels,high expression in the IL-10 levels were detected in the SLE group. TNFα was upregulated in the NAFL+auto group at both the protein and transcriptional levels with negative correlation with IL-10. The AST levels were significantly elevated Summary 99 only in RA patients, with no significant changes in the ALT level among various patients’ groups. TLR3 was shown to be unable to differentiate between HCV and NAFL patients at both the protein and mRNA levels. Beneficially, TLR3 can differentiate between NAFL and NAFL+auto at the protein level. Importantly, at the protein level, TLR7 can well differentiate between HCV and NAFL patients. At the transcription level, the TLR7 can also differentiate between the NAFL and the NAFL+auto patients, since a significantly higher expression of TLR7 in the NAFL+auto patients compared to healthy individuals, HCV, HCV+auto, NAFL, SLE or RA patients was observed. Last and not least, TLRs 3 and 7 can differentiate between the NAFL and NAFL+auto patients. Further investigations needed to elucidate whether both TLR 3 and TLR 7 signaling mechanisms worked in tandem together to establish an antiviral state in HCV infected individuals. |