期刊
ACTA DERMATO-VENEREOLOGICA
卷 94, 期 1, 页码 26-31出版社
ACTA DERMATO-VENEREOLOGICA
DOI: 10.2340/00015555-1650
关键词
TNF; infliximab; interferon-gamma; cellular immune response; psoriasis
类别
资金
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [08/57608-2]
Treatment of patients with immune-mediated inflammatory diseases with anti-tumour necrosis factor (anti-TNF) agents increases the risk of tuberculosis reactivation, suggesting that it may affect their cellular immune responses. We evaluated cellular immune responses of 12 severe psoriasis patients before and during infliximab treatment. Peripheral blood mononuclear cells were stimulated with phytohaemagglutinin, the superantigen enterotoxin B (SEB), a cytomegalovirus lysate (CMV), and Mycobacterium tuberculosis (Mtb) antigens. The lymphocyte proliferative and IFN-gamma responses were evaluated. Treatment with infliximab did not lead to reduction in the IFN-gamma and lymphoproliferative responses: it rather increased the overnight release of IFN-gamma in phytohaemagglutinin and SEB stimulated cultures. This effect was most noted at the peak of the anti-TNF clinical effect and less prominent at its nadir. Immunoreactivity to CMV was also either unaffected or slightly increased by the anti-TNF. Of note, the IFN-gamma and proliferative responses to Mtb by the two tuberculin skin test-reactors were also increased at the peak of infliximab, declining at its nadir. The deleterious consequences of TNF blockade in severe psoriasis patients undergoing infliximab treatment are apparently attenuated by the abbreviation of the immunosuppressive effect of TNF overexpression.
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