Natural killer cell activity from hemophiliacs exhibits differential
responses to various forms of interferon
DS Matheson, BJ Green, MC Poon, MJ Fritzler, DI Hoar and TJ Bowen
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- beta (IFN-beta). It is
feasible that chronic antigen stimulation with subsequent release of
interferon could be related to the impaired NK reactivity to IFN-beta 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-alpha, IFN-beta
and IFN-gamma 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-alpha by increasing NK activity, but four patients had significant
failure and two had mild impairment in NK response to IFN-beta. This latter
observation was particularly evident at very low concentrations of IFN. In
repeated experiments, seven of eight had impaired NK response to IFN-beta
and IFN-gamma but normal response to IFN-alpha. Only one patient's NK cells
responded better to IFN-gamma. 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.
Volume 67,
Issue 1,
pp. 164-167,
01/01/1986
Copyright © 1986 by The American Society of Hematology
