Spontaneous cell proliferation is associated with poor sensitivity to glucocorticoids in patients infected with HTLV.
Cell Prolif
; 40(1): 64-74, 2007 Feb.
Article
en En
| MEDLINE
| ID: mdl-17227296
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Dexametasona
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Linfocitos T
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Infecciones por HTLV-I
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Infecciones por HTLV-II
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Glucocorticoides
Tipo de estudio:
Diagnostic_studies
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Observational_studies
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Risk_factors_studies
Límite:
Adolescent
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Adult
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Aged
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Cell Prolif
Año:
2007
Tipo del documento:
Article
País de afiliación:
Brasil
Pais de publicación:
Reino Unido