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Polymorph-mediated antibody-dependent cytoxicity--modulation of activity by drugs and immune interferon
Abstract:
Bovine polymorphonuclear leukocytes (PMN) mediated antibody-dependent cell cytotoxicity (ADCC) against erythrocyte and herpes virus-infected target cells. The extent of cytotoxicity was not affected by drugs that inhibited DNA, RNA, or protein synthesis. The effect did not occur in the absence of divalent cations, was suppressed by pretreatment of PMN with silica and cytochalasin B, and was subject to the bidirectional control by cyclic nucleotides; drugs decreasing cyclic AMP or elevating cyclic GMP levels enhanced ADCC. The ADCC phenomena was also enhanced by supernates containing immune interferon activity from antigen-stimulated-immune lymphocyte-macrophage cultures. The possibility that immune interferon(s) might be causing the elevation of ADCC and the relevance of this observation in terms of the part interferon might play in modulating recovery from herpes virus infections was discussed.
Insights
Bovine polymorphonuclear leukocytes (PMN) exhibit antibody-dependent cell cytotoxicity (ADCC) against infected cells. Immune interferon enhances this activity, suggesting a role in herpes virus infection recovery.
Area of Science:
- Immunology
- Cellular Biology
- Virology
Background:
- Bovine polymorphonuclear leukocytes (PMN) play a role in immune responses.
- Antibody-dependent cell cytotoxicity (ADCC) is a key mechanism of cell-mediated immunity.
- Herpes virus infections pose significant challenges in cattle.
Purpose of the Study:
- To investigate the capacity of bovine PMN to mediate ADCC against erythrocyte and herpes virus-infected cells.
- To explore factors influencing bovine PMN-mediated ADCC, including chemical inhibitors and immune mediators.
- To assess the potential role of immune interferon in modulating ADCC and its implications for herpes virus infections.
Main Methods:
- Assessing ADCC activity of bovine PMN against target cells.
- Evaluating the impact of DNA, RNA, and protein synthesis inhibitors on ADCC.
- Investigating the requirement for divalent cations and the effect of PMN pretreatment with silica and cytochalasin B.
- Examining the influence of cyclic nucleotides (cAMP, cGMP) on ADCC.
- Assessing the enhancement of ADCC by immune interferon-containing supernates.
Main Results:
- Bovine PMN mediated ADCC against target cells, independent of DNA, RNA, or protein synthesis.
- ADCC was dependent on divalent cations and inhibited by silica and cytochalasin B.
- Cyclic nucleotides bidirectionally controlled ADCC, with decreased cAMP or elevated cGMP enhancing the response.
- Immune interferon-containing supernates significantly enhanced ADCC activity.
Conclusions:
- Bovine PMN possess potent ADCC capabilities against infected cells.
- Immune interferon may play a crucial role in enhancing ADCC, potentially impacting recovery from herpes virus infections.
- The findings highlight the complex regulatory mechanisms of PMN-mediated cytotoxicity and its relevance in antiviral immunity.