Immunohistological examination of long term changes of the t-cell mediated immune response in Egyptian patients with chronic hepatitis C with and without <i>Schistosoma mansoni</i> infection

Abstract

The host immune response is playing a key role in liver injury occurring in patients with chronic hepatitis C or schistosomiasis or in case of coinfection. The rational of the current study is to investigate the cell mediated immunity in the liver of patients with or without cirrhosis due to hepatitis C or schistosomiasis or both. The CD3 (Tlymphocytes), CD4 (helper/inducer T-cells), CD8 (suppressor/cytotoxic T-cells), CD11b, and CD16 (NK activity) were counted immunohistochemically in liver samples using specific monoclones in four patient groups, non-cirrhotic patients free of schistosomiasis with hepatitis C (Group I), non- cirrhotic patients coinfected with schistosomiasis and hepatitis C (Group II), cirrhotic patients free of schistosomiasis with hepatitis C (Group III), and cirrhotic patients coinfected with both schistosomiasis and hepatitis C (Group IV). The results showed that there is a significant difference between the four groups of patients regarding CD4 count. Patients without schistosoma coinfection and without cirrhosis (Group I) showed significantly (P < 0.001) risen counts of CD4+ compared to patients with coinfection and cirrhotic remodelling (Group IV). For patients suffering from liver cirrhosis (Group III) significantly elevated levels of CD4+ lymphocytes (P = 0.014) were detectable compared to patients already suffering from liver cirrhosis and coinfection (Group IV). The counted CD4 cells in chronic hepatitis C group without S. mansoni infection (group one) was found elevated versus the count of CD4 cells in the group with the coinfection (group two) and this was statistically significant (P = 0.01). The CD8 count was statistically highly significant between the four groups. CD8 cells count in the two groups with the coinfection was found elevated against the other two groups with HCV infection only. On the other hand, the patients coinfected with schistosome without cirrhosis (Group II) and with cirrhosis (Group IV) showed a significant elevation of CD8 versus patients infected with HCV only without cirrhosis (Group I) (P = 0.001) & (P < 0.0001) respectively.
Moreover, the patients coinfected with schistosome with cirrhosis (Group IV) showed a significant elevation of CD8 versus patients infected with HCV only with cirrhosis (Group III) (P = 0.022). The obtained CD4/8 ratio was decreased in coinfected versus the nonconifected patients. The CD3, CD11b, and CD16 cells counts were non-significantly different among the four groups. Collectively, the schistosome coinfection increases the level of CD8 and decreases the CD4 count in livers of cirrhotic and non-cirrhotic patients. In conclusion, the progression of liver diseases is associated with a dysregulation of cellular immune responses. T-lymphocytes cells may
play a role in the immunopathogenesis of liver cirrhosis in patients with HCV and severely in coinfected patients with both hepatitis C and schistosomiasis.

Key Words: Cellular Immunity, HCV, Schistosomiasis, Liver Cirrhosis.