SUMMARYSpecific polyclonal antisera to human interferon-~l (HulFN-~I), human interferon-~2 (HulFN-~2) and human lymphoblastoid interferon (HulFN-ctLy Namalwa) have been raised in rabbits and sheep. The antisera raised against HulFN-~I and HulFN-~2 strongly neutralized the antiviral activity of their homologous IFN-~ subtypes, but were less active against the heterologous IFN-~ subtypes and preparations containing mixtures of IFN-~ subtypes, e.g. human leukocyte interferon (HulFN-aLe). Antisera raised against HulFN-aLy Namalwa strongly neutralized the antiviral activity of all IFN-~-containing preparations and showed weak cross-reactivity with human interferon-fl (HulFN-fl). Neither anti-HulFN-~l nor anti-HulFN-~2 could be demonstrated to neutralize the antiviral activity of HulFN-fl. A number of monoclonal antibodies to HulFN-a2 have been prepared and these were found to neutralize HulFN-~2 antiviral activity to varying degrees, but not to neutralize the heterologous subtype HulFN-~ 1, preparations containing mixtures of IFN-~ subtypes or HulFN-fl.

The role of interferon (IFN) gamma in controlling chronic infections of Listeria monocytogenes (Listeria) was studied in athymic C57BL/6 nu/nu mice, and by treating thymectomized C57BL/6 +/+ mice with monoclonal rat CD4 and CD8-specific monoclonal antibodies (Mab). Mice treated with a combination of the two T cell subset antibodies were similar to athymic, nude mice in being able to control Listeria infection, keeping the titers below 3-5 log10 bacteria per organ, but they could not eliminate them completely. Treatment with antibodies to IFN gamma of nude or CD4+ + CD8+ - T cell-depleted mice suffering from chronic Listeria infection caused a marked increase of Listeria titers in liver and spleen. This result implies a role of IFN gamma in maintaining anti-Listeria resistance in mice lacking mature T cells.