Open AccessSpontaneous cell proliferation is associated with poor sensitivity to glucocorticoids in patients infected with HTLV
Author(s) -
Lopes R. P.,
MennaBarreto M.,
Bauer M. E.
Publication year - 2007
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.2007.00419.x
Subject(s) - dexamethasone , cell growth , immunology , glucocorticoid , in vitro , t cell , medicine , stimulation , cell , biology , virology , immune system , biochemistry , genetics
. Background : Human T‐cell lymphotropic viruses (HTLV)‐I/II have a special tropism for infecting T cells and inducing spontaneous lymphocyte proliferation. Leukaemia and neurological manifestations are associated with HTLV‐I/II infections, and treatment is usually based on anti‐inflammatory drugs including glucocorticoids. Although steroid resistance has been reported, it is unknown whether this condition is related to the infection itself or to the treatment. Objective : We investigated whether spontaneous cell proliferation is associated with T‐cell sensitivity to glucocorticoids. Materials and Methods : Twenty‐eight HTLV‐I/II patients and 11 healthy age‐matched controls took part in this study. Lymphocytes were isolated and cultured in vitro to measure spontaneous and mitogen‐induced proliferation as well as cellular sensitivity to dexamethasone. Results : Patients with HTLV‐I/II infection showed similar stimulated and unstimulated T‐cell proliferation as well as comparable sensitivity to dexamethasone in vitro . There were no group differences in the frequency of glucocorticoid responders versus non‐responders. However, T cells of patients with spontaneous proliferation were unresponsive to mitogenic stimulation and were remarkably more resistant to dexamethasone than cells of patients with normal proliferation. Conclusion : These data suggest that the poor clinical response to steroids may be associated with spontaneous cell proliferation during HTLV infection.