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Deficient interleukin 2 dependent proliferation pathway in T lymphocytes from active and inactive ulcerative colitis patients.
  1. L Manzano,
  2. M Alvarez-Mon,
  3. J A Vargas,
  4. J A Girón,
  5. L Abreu,
  6. A Fernández-Corugedo,
  7. L I Román,
  8. F Albarran,
  9. A Durántez
  1. Department of Medicine, Hospital Universitario Prínciple de Asturias, Universidad de Alcalá, Madrid, Spain.

    Abstract

    There is increasing evidence that ulcerative colitis is associated with an abnormality of the immune system. Although the aetiology remains unknown, it has been suggested that the immune system of these patients is implicated in the pathogenesis of their disease. T cell function was investigated in ulcerative colitis patients and defective phytohaemagglutinin induced T cell mitogenesis was found. The DNA synthesis induced by stimulation with phorbol esters plus ionophore (ionomycin), however, was normal. These changes cannot be ascribed to either decreased interleukin 2 synthesis or to a defective interleukin 2 receptor expression after cellular activation. Moreover, this defective proliferative response of the T lymphocytes was observed even in the presence of saturated concentrations of exogenous interleukin 2. These results emphasise that the interleukin 2 dependent proliferation pathway is deficient in T lymphocytes from ulcerative colitis patients.

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