Interferon-gamma (IFN-gamma) exerts a broad spectrum of activities which affect the responses of mature B-cells. It strongly inhibits B-cell activation, acts as a B-cell growth factor (BCGF), and also induces final differentiation to immunoglobulin (Ig) production. IFN-gamma is deeply involved in the differential control of isotype expression, as it enhances IgG2a production and suppresses both IgG1 and IgE production. Although it is now possible to draw a general scheme of the effects of IFN-gamma on B-cells, a number of paradoxical results still exist in the field. In this manuscript, different experimental systems are analyzed in an attempt to explain these apparent paradoxes.
T lymphocytes from 21 untreated patients with acute brucellosis were tested for their proliferative response to polyclonal mitogens. The purified T lymphocytes from these patients showed a defective proliferative response to plant lectins and anti CD3 monoclonal antibodies with respect to the response observed in T lymphocytes from 21 healthy controls (p < 0.05). This defective proliferative response was not corrected by the exogenous addition of interleukin-2 or tumor necrosis factors alpha or beta to the culture medium. After antibiotic therapy, the proliferative response to the mitogens in T lymphocytes was found to be similar to that of the healthy controls (p > 0.05), and significantly higher than that found before treatment (p < 0.05). It was concluded that T lymphocytes from acute brucellosis patients have a defective proliferative response to membrane mitogenic signals, which disappears when the patients are cured after antibiotic treatment.
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