Natural Killer Cell Activity From Hemophiliacs Exhibits Differential Responses to Various Forms of Interferon

• Published in: Blood Vol. 67; no. 1; pp. 164 - 167
• Main Authors: Matheson, David S., Green, Bridget J., Poon, Man-Chiu, Fritzler, Marvin J., Hoar, David I., Bowen, Thomas J.
• Format: Journal Article
• Language: English
• Published: Washington, DC Elsevier Inc 01-01-1986; The Americain Society of Hematology
• Subjects: Adult; AIDS/HIV; Biological and medical sciences; Hematologic and hematopoietic diseases; Hemophilia A - immunology; Humans; Interferons - pharmacology; Killer Cells, Natural - drug effects; Killer Cells, Natural - immunology; Male; Medical sciences; Middle Aged; Platelet diseases and coagulopathies; Receptors, Immunologic - analysis; Receptors, Interferon; T-Lymphocytes - immunology; Virus; Natural killer cell; Human; Antibody; Hemophilia; Retroviridae; AIDS; Hemopathy; Interferon; HTLV-III virus; Coagulopathy
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V67.1.164.164

Patients with hemophilia are at risk for the development of acquired immunodeficiency syndrome (AIDS). Patients with AIDS have recurrent infections and/or malignancy and altered immune response, including decreased T lymphocyte counts, decreased T helper lymphocytes, defective T cell blastogenesis, hypergammaglobulinemia, defective natural killer (NK) activity and impaired response of NK to interferon-0 (IFN-0). It is feasible that chronic antigen stimulation with subsequent release of interferon could be related to the impaired NK reactivity to IFN-ß of patients with AIDS. Because hemophiliacs are subjected to chronic antigen stimulation secondary to the administration of foreign protein, the reactivity of NK cells from patients with hemophilia to IFN-a, IFN-ß and IFN-7 was studied. Eight patients with hemophilia requiring high levels of clotting factor replacement were assessed. Three patients were antibody positive to HTLV-III. All had normal baseline NK cell function. In the first set of experiments, all patients responded normally to in vitro IFN-a by increasing NK activity, but four patients had significant failure and two had mild impairment in NK response to IFN-ß. This latter observation was particularly evident at very low concentrations of IFN. In repeated experiments, seven of eight had impaired NK response to IFN-ß and IFN-7 but normal response to IFN-a. Only one patient's NK cells responded better to IFN-7. There was no obvious correlation of these findings to antibody status to HTLV-III. Chronic antigen stimulation and the modulation of interferon receptors are discussed as possible mechanisms that could produce these findings.