الفهرس 
Hepatitis C VirusOnly 14 pages are availabe for public view
 |  | from | 145 |  |  |
| | | from | 145 | | |
Abstract
The killer cell immunoglobulin-like receptors (KIR) control the
activation or inhibition of Natural killer (NK) cells by recognition of
specific HLA class I ligands, such that target cell cytolysis occur only
when activating signals overcome inhibitory signals. The aim of the study
is to demonstrate the effect of HLA class I and KIR2DL2 and KIR3DL1
gene expression interaction on the outcome of HCV infection. Material
and methods: The study included (33) chronic HCV patient undergone
liver transplantation; and (33) adults healthy control. Both the patients
and controls are subjected to assessment of (KIR2DL2 and KIR3DL1)
gene expression in peripheral blood (PB) and liver tissue by real time
polymerase chain reaction( PCR). Moreover, HLA typing of class HLAC
for the patient group (33) and for (138) healthy subject as control group
were done by sequence specific oliguonucleotides (SSOP) technique
utilizing methodology of sequence specific oliguonucleotides probe.
results:KIR2DL2 shows significantly high expression in tissue of the
patient group compared to the control group with (Pvalue=
0.02),regarding the patient group the KIR2DL2 gene expression in the
tissue significantly increase relative to its PB with (P value=0.04).While
in the control group no significant difference was observed (P>0.05).On
the other hand ,KIR3DL1 gene expression showed no significant
difference between the patient and control group, as well as no significant
difference was noticed within the patient neither control group(P>0.05).
concerning HLA-C typing ,HLA –C1C2 was the most common HLA-C
type however no significantly difference between the patients and
controls with (P>0.05)conclusion :this study can contribute to the further
prospective study with larger scale suggesting the assumption that
KIR2DL2 might hampered HCV clearance by inhibiting NK cell killing
function affecting both innate and acquired immune response.