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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Abnormal gamma IFN and alpha TNF secretion in purified CD2+ cells from autoimmune thrombocytopenic purpura (ATP) patients: their implication in the clinical course of the disease.

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. Abnormalities in the production of these cytokines may be involved in the clinical course of autoimmune thrombocytopenic purpura (ATP). This paper describes the production of these cytokines in PHA-stimulated peripheral blood CD2+ cells from ATP patients. Both gamma IFN and alpha TNF were significantly increased in PHA-stimulated CD2+ cells from therapy-dependent ATP patients (platelet counts < 50,000/microliter), as compared to ATP patients with stable disease (sustained platelet counts < 50,000/microliter without need treatment) (P < 0.05). No significant differences were found in gamma IFN production by PHA-stimulated CD2+ cells between therapy-dependent ATP patients and healthy controls (P < 0.05). However, the production of alpha TNF by PHA-stimulated CD2+ cells from therapy-dependent ATP patients was significantly higher compared to that found in healthy controls (P < 0.05). There were no significant differences in IL-6 production by PHA-stimulated CD2+ cells from ATP patients and healthy controls (P < 0.05). These findings demonstrate abnormal gamma IFN and alpha TNF secretion in purified CD2 cells from ATP patients. The clinical severity of the disease is associated with the altered secretion of these lymphokines by CD2 cells.[1]

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