451. Evidence for prostaglandin-producing supressor cells in HCV patients with normal ALT.
- Author
-
Marinho R, Pinto R, Santos ML, and de M
- Subjects
- Carcinoma, Hepatocellular enzymology, Carcinoma, Hepatocellular immunology, Carrier State enzymology, Carrier State immunology, Dinoprostone antagonists & inhibitors, Hepatitis C Antigens immunology, Hepatitis C, Chronic drug therapy, Hepatitis C, Chronic enzymology, Humans, Indomethacin pharmacology, Liver enzymology, Liver Neoplasms enzymology, Liver Neoplasms immunology, Lymphocyte Activation, T-Lymphocytes, Regulatory metabolism, Alanine Transaminase blood, Dinoprostone biosynthesis, Hepatitis C, Chronic immunology, T-Lymphocytes, Regulatory immunology
- Abstract
Our objective was to verify the presence of prostaglandin-producing suppressor cells in response to hepatitis C virus antigens in peripheral blood mononuclear cells proliferation. Standard proliferation tests were performed in 31 patients: 20 with chronic hepatitis C after antiviral treatment [7 long-term responders (LTR), 7 relapsers (RR), 6 nonresponders (NR)], 7 with HCV infection with persistently normal aminotransferase levels (PNAL), and 4 with hepatocellular carcinoma. Six antigens were used from the core and NS3 regions. A modified proliferation assay consisting of the addition of indomethacin was also done. Lymphoproliferative responses to the HCV antigens were detectable in 27% (11/41) of test points of LTR, 10% (3/31) of RR, 26% (9/35) of NR, and 18% (7/39) of patients with PNAL. Indomethacin only had effect in PNAL patients, by increasing the frequency of reactivity from 18% (7/39) to 36% (14/39) tests points (P = 0.037); also, in three of these patients (43%) indomethacin strongly modified proliferation to core 31-50 and NS3 1248-1261 antigens, increasing both the frequency and stimulation index from 33% (6/18) to 72% (13/18) (chi2 = 5.43, P = 0.019) and 1.89 +/- 0.43 to 6.18 +/- 4.74 (P = 0.028), respectively. These results suggest that prostaglandin-producing suppressor may play a role in chronic HCV infection by inhibiting cellular immune responses in patients with persistently normal ALT.
- Published
- 2002
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