IFN-beta impairs superoxide-dependent parasite killing in human macrophages: evidence for a deleterious role of SOD1 in cutaneous leishmaniasis.

Type I IFNs (IFN-alpha/beta) have only recently gained considerable attention as immunomodulators in nonviral infectious diseases. IFN-beta has been shown to protect, in a NO-dependent manner, against murine Old World leishmaniasis caused by Leishmania major, but data in New World leishmaniasis are lacking. We found that IFN-beta dose-dependently increases parasite burden in Leishmania amazonensis- as well as Leishmania braziliensis-infected human macrophages, independent of endogenous or exogenous NO.

Interferon, a growing cytokine family: 50 years of interferon research.

The establishment of an antiviral state in cells is the defining activity of interferons (IFNs) as well as the property that permitted their discovery in 1957 by Isaacs and Lindenmann. In addition, interferons have other cellular functions that have potential clinical applications. Today, interferons are used for the treatment of a variety of malignancies and viral diseases.

Alterations in interferon-gamma and nitric oxide levels in human echinococcosis.

Human cystic hydatid disease is characterized by the long-term coexistence of Echinococcus granulosus and its host without effective rejection of the parasite. This parasitic helminth infection currently constitutes a major health problem in Algeria. We investigated interferon-gamma (IFN-gamma) and nitrite (NO2-) production in PBMC culture 2 supernatants from Algerian patients (n = 35), stimulated by a major antigen (antigen 5).

Downregulation of angiogenic factors in Ewing tumor xenografts by the combination of human interferon-alpha or interferon-beta with ifosfamide.

Ewing sarcoma is the second most common bone tumor in childhood. Despite aggressive chemotherapy and radiotherapy, the prognosis of metastatic disease remains poor. In a nude mouse model of Ewing tumor xenografts, we recently showed that human type I interferons (IFNs) inhibit the growth of established xenografts.

NF-kappaB activation prevents apoptotic oxidative stress via an increase of both thioredoxin and MnSOD levels in TNFalpha-treated Ewing sarcoma cells.

Repression of activation of c-Jun N-terminal kinase (JNK) participates in the anti-apoptotic effect of nuclear factor-kappaB (NF-kappaB) in TNFalpha-treated Ewing sarcoma cells. As oxidative stress is one of the most prominent activators of JNK, we investigated the relationship between TNFalpha-induced NF-kappaB activation and the control of oxidative stress. Inhibition of NF-kappaB activation resulted in an increase in TNFalpha-induced ROS production, lipid peroxidation and protein oxidation.