ABNORMAL GAMMA-IFN AND ALPHA-TNF SECRETION IN PURIFIED CD2- THEIR IMPLICATION IN THE CLINICAL COURSE OF THE DISEASE( CELLS FROM AUTOIMMUNE THROMBOCYTOPENIC PURPURA (ATP) PATIENTS )
J. Garciasuarez et al., ABNORMAL GAMMA-IFN AND ALPHA-TNF SECRETION IN PURIFIED CD2- THEIR IMPLICATION IN THE CLINICAL COURSE OF THE DISEASE( CELLS FROM AUTOIMMUNE THROMBOCYTOPENIC PURPURA (ATP) PATIENTS ), American journal of hematology, 49(4), 1995, pp. 271-276
Gamma inferferon (gamma IFN), alpha tumor necrosis factor (alpha TNF),
and interleukin 6 (IL-60) are cytokines produced by a wide variety of
cells, including T lymphocytes and NK cells, These cytokines affect B
-cell proliferation and differentiation into immunoglobulin secreting
cells. In addition, gamma IFN and alpha TNF also enhance the function
of macrophages, upregulating the expression of their IgG receptors, Ab
normalities in the production of these cytokines may be involved in th
e clinical course of autoimmune thrombocytopenic purpura (ATP), This p
aper describes the production of these cytokines in PHA-stimulated per
ipheral blood CD2+ cells from ATP patients. Both gamma IFN and alpha T
NF were significantly increased in PHA-stimulated CD2+ cells from ther
apy-dependent ATP patients (platelet counts <50,000/)mu l), as compare
d to ATP patients with stable disease (sustained platelet counts >50,0
00/mu l without need treatment) (P < 0.05), No significant differences
were found in gamma IFN production by PHA-stimulated CD2+ cells betwe
en therapy-dependent ATP patients and healthy controls (P < 0.05). How
ever, the production of alpha TNF by PHA-stimulated CD2+ cells from th
erapy-dependent ATP patients was significantly higher compared to that
found in healthy controls (P < 0.05), There were no significant diffe
rences in IL-6 production by PHA-stimulated CD2+ cells from ATP patien
ts and healthy controls (P < 0.05), These findings demonstrate abnorma
l gamma IFN and alpha TNF secretion in purified CD2 cells from ATP pat
ients, The clinical severity of the disease is associated with the alt
ered secretion of these lymphokines by CD2 cells. (C) 1995 Wiley-Lies,
Inc.