作者: S J Till , Christopher Corrigan , J North , J Barkans , David Robinson
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摘要: Atopic allergic asthma is characterized by activation of Th2-type T cells in the bronchial mucosa. Previous reports have suggested an important role for costimulation through CD28/CTLA4-CD80/CD86 pathway allergen animal models inhaled challenge. However, human allergen-specific lines and clones were reported to be independent. We therefore examined CD80 CD86 dependence allergen-induced cell proliferation cytokine production peripheral blood bronchoalveolar lavage from atopic asthmatic subjects controls. Both IL-5 PBMC inhibited CTLA4-Ig fusion protein anti-CD86, but not anti-CD80 mAbs. When CD4+ examined, found independent or costimulation. when obtained directly airways was anti-CD86 anti-CD80. In addition, lavage-adherent asthmatic, control showed APC activity autologous cells. This also Thus airway susceptible blockade agents interfering with via CD86, this may hold therapeutic potential asthma.