Biomedical subjects

H Wedemeyer

Publications and source records attributed to H Wedemeyer.

39 records · Page 3Linked to original sources

PubMedDate not supplied

Effects of cyclosporine on human dendritic cell subsets.

Cyclosporine is widely used as an immunosuppressive agent after solid organ transplantation. Limited data are available on the modulation of human dendritic cells by cyclosporine. We investigated the effects of cyclosporine on the phenotype and function of human dendritic cell (DC) subsets. DCs were isolated from peripheral blood using magnetic bead-conjugated antibodies. Cyclosporine did not alter the ability of myeloid and plasmacytoid dendritic cells to take up antigens. Expression of the co-stimulatory molecule CD80 but not CD86 increased on both DC subsets when stimulated with cyclosporine. The ability of cyclosporine treated myeloid DCs to stimulate proliferation of allogenic PBMC was significantly reduced. Similarly, stimulation of memory CD8+ T cells by dendritic cells was impaired by cyclosporine pretreatment. In conclusion, cyclosporine differentially alters function and phenotype of myeloid dendritic cells leading to a partially impaired capacity to stimulate allogenic and autologous T cells.

Cell Division↗

PubMedDate not supplied

Hepatitis C: therapeutic perspectives.

Continuous efforts are vital to develop new treatment strategies to improve sustained response rates, especially for difficult to treat patients infected with the hepatitis C virus. Despite the introduction of ribavirin, more than 50% of the patients do not eliminate the virus with the current standard therapy of interferon-a (IFN) and ribavirin. Options to further enhance response rates include modification of the IFN-dosing schedule with daily dosing of IFN, new IFN such as consensus interferon or modified IFN with longer half-life and more favourable pharmacokinetics such as pegylated IFN (PEG-IFN). Clinical trials with new IFN showed that consensus IFN may improve response rates in unsuccessfully pre-treated patients and patients with HCV-genotype-1. Treatments with PEG-IFN will double response rates achieved with standard IFN monotherapy. The combination of PEG-IFN and ribavirin improves the virological response to more than 50% and even to more than 80% in patients with genotype 2 or 3. By now, standard therapy of chronic hepatitis C has been changed to the combination of PEG-IFN plus ribavirin. Future anti-viral drugs may comprise molecules that directly inhibit HCV proteins and interfere with viral replication. NS3/4A serine protease, ribonucleic acid (RNA) helicase, RNA-dependent RNA polymerase may be potential targets for new drugs. Furthermore antisense oligonucleotides or ribozymes may become new treatment options to inhibit HCV replication. Finally, immunotherapies to enhance HCV-specific immune responses are also attractive strategies to control HCV infection and to prevent chronic liver disease.

Antiviral Agents↗

PubMedDate not supplied

Perihepatic lymphadenopathy: a marker of response to interferon alpha in chronic hepatitis C.

BACKGROUND/AIMS: Recently it was shown that perihepatic lymphadenopathy (PHL) correlates with histological activity in chronic hepatitis C. However, the question whether there is a correlation between the response to interferon alpha and PHL has not yet been raised. METHODOLOGY: We examined 103 patients who had been treated with interferon alpha for hepatitis C. Prior to treatment all patients had undergone high resolution ultrasonography. Thirty-six patients had follow up ultrasound scans during the course of the treatment. According to size and number of lymph nodes we introduced a grading of the PHL and determined grade I as minimal, grade II as medium and grade III as extensive PHL. RESULTS: Classification of PHL prior to treatment revealed 40 patients with PHL I, 30 with grade II and 33 with grade III. Hepatic inflammatory activity according to the Ishak score was increased in patients with PHL III (9.1+/-2.4) compared to PHL II (6.7+/-2.9) and PHL I (7.3+/-3.1) (p=0.01). In patients with PHL grade I prior to treatment 45% were initial responder, patients with grade II or III showed response rates of 40% and 33%, respectively. During therapy we found an increase of PHL in one out of 13 primary responder vs. 10 out of 23 non-responder (p=0.03). CONCLUSIONS: In conclusion, monitoring of PHL by abdominal ultrasonography is a simple, non-invasive and cheap additional marker of response to interferon alpha.

Adolescent↗