A Major Role of Macrophage Activation by Interferon-Gamma during Mouse Hepatitis Virus Type 3 Infection. I. Genetically Dependent Resistance
| Autor: | Carlos Eduardo Pereira, Lucchiari Ma |
|---|---|
| Rok vydání: | 1989 |
| Předmět: |
Lipopolysaccharides
T-Lymphocytes medicine.medical_treatment Immunology Mice Inbred Strains Spleen Biology Antibodies Viral Article Virus Interferon-gamma Mice Mouse hepatitis virus Interferon Concanavalin A FCS fetal calf serum PFU plaque-forming units medicine Animals MHV3 mouse hepatitis virus type 3 Immunology and Allergy IFN interferon Interferon gamma Con A concanavalin A Cells Cultured Murine hepatitis virus Macrophages MФ macrophage(s) Hematology Macrophage Activation i.p. intraperitoneally biology.organism_classification Virology Immunity Innate Cytokine medicine.anatomical_structure Viral replication Cell culture Hepatitis Viral Animal LPS lipopolysaccharide medicine.drug |
| Zdroj: | Immunobiology |
| ISSN: | 0171-2985 |
| DOI: | 10.1016/s0171-2985(89)80026-9 |
| Popis: | Resistance of mice to mouse hepatitis virus type 3 (MHV3) infection is genetically determined. Normal adult A/J mice are resistant, and BALB/c mice are susceptible. Higher titers of virus and interferon (IFN) in vivo were found in MHV3-infected BALB/c mice compared with A/J mice. In vitro activation of macrophages (M phi) by lipopolysaccharide (LPS) delayed MHV3 replication only in cells that originated from A/J mice, although cell populations from both A/J and BALB/c mice were able to synthesize comparable amounts of IFN-alpha/beta. Using specific antibodies, we have shown that the delayed MHV3 replication in LPS-activated A/J M phi was due, in part, to IFN-alpha/beta. A/J M phi were found to be more sensitive to IFN-gamma than to IFN-alpha/beta, and BALB/c M phi did not develop an antiviral state to either IFN. Cultured spleen cells from A/J mice synthesized more IFN-gamma than BALB/c spleen cells after specific or non-specific stimulation. The results indicate that IFN-activated M phi may play a crucial role in the resistance to MHV3 infection. Since IFN-gamma is produced in large amounts by A/J spleen cells after specific stimulation with MHV3 and is efficient in activating the A/J M phi, a T cell-dependent mechanism is likely to be involved. |
| Databáze: | OpenAIRE |
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