Autoimmune diseases are connected with disturbances in cytokine synthesis, and therapy with IFN-gamma blockers is their main pathogenetic treatment.

Development of autoimmune process in the organism is mainly due to disturbances in cytokine production. Hyperproduction of cytokines can be induced by certain viruses, bacteria, genetic factors, and other triggers. Cytokines act in an interrelated immune cascade with interferon-gamma (IFN-gamma) playing a central role.

Anticytokine therapy, especially anti-interferon-gamma, as a pathogenetic treatment in TH-1 autoimmune diseases.

We pioneered anticytokine therapy (ACT) in 1974 and 1989, proposing to remove interferon (IFN) and tumor necrosis factor (TNF)-alpha together with IFNs to treat various autoimmune diseases, including AIDS. This hypothesis was confirmed in different laboratories and opened a new line to produce and test different anticytokines. We have had good, sometimes striking results treating various Th1-mediated autoimmune diseases, including inflammatory skin diseases, using anti-IFN-gamma and sometimes anti-TNF-alpha.

Anticytokine therapy, particularly anti-IFN-gamma, in Th1-mediated autoimmune diseases.

Anticytokine therapy was proposed in 1974 in Nature, in which it was stated that hyperproduced interferon can cause autoimmune disease and anti-interferon can be therapeutic. In 1989, the use of antibodies to tumor necrosis factor-alpha in combination with antibodies to certain types of interferon was proposed to treat various autoimmune diseases, including AIDS. The first anticytokine therapy was conducted in 1975.

Anti-interferon-gamma antibodies in the treatment of autoimmune diseases.

Interferon (IFN)-gamma is an important immune regulator in normal immunity. When IFN gamma production is disturbed, various autoimmune diseases (ADs) can develop, in which we suggest that anti-IFN gamma could have a beneficial effect. Depending on the cell type in which IFN gamma synthesis is disturbed, different clinical manifestations may result.

Treatment of corneal transplant rejection in humans with anti-interferon-gamma antibodies.

Purpose: To determine efficacy of anti-human interferon-gamma F(ab')2 (Fabs) in treating corneal transplant rejection after penetrating keratoplasty.

Design: Interventional case series.

Methods: Anti-interferon-gamma Fabs derived from goat antihuman interferon-gamma antibodies were used for instillations in 13 patients (13 eyes) who experienced corneal transplant rejection after penetrating keratoplasty.