HLA-DR+CD38+ activated Th17.1 cells reflect disease activity and corticosteroid responsiveness in pulmonary sarcoidosis

BACKGROUND: T cells following exposure to unknown antigens. Th17.1 cells appear to play important roles in the pathophysiology of pulmonary sarcoidosis by differentiating from Th17 cells through interactions with antigen-presenting cells and producing large amounts of interferon gamma. However, whether these cells promote or inhibit granulomatous inflammation and how regulatory T cells, which suppress the activity of these cells, are involved in the pathogenesis of sarcoidosis remains unclear. This exploratory study aimed to elucidate the roles of Th17.1 cells and regulatory T cells in the pathophysiology of pulmonary sarcoidosis. METHODS: We compared and evaluated the proportions and activation states of Th17.1 cells and regulatory T cells in peripheral blood (n = 34) and bronchoalveolar lavage fluid (n = 22) from patients with pulmonary sarcoidosis, and from patients with connective tissue disease-associated interstitial lung disease (n = 36, 34). We also conducted a longitudinal investigation of changes before and after corticosteroid treatment and associations with disease progression. RESULTS: The proportion of activated Th17.1 cells was higher in peripheral blood and bronchoalveolar lavage fluid from patients with pulmonary sarcoidosis than from patients with connective tissue disease-associated interstitial lung disease. However, this proportion decreased with corticosteroid administration and was associated with disease progression. The proportion of regulatory T cells was significantly lower in the lungs of sarcoidosis patients compared to those with connective tissue disease-associated interstitial lung disease. CONCLUSION: Among patients with corticosteroid-responsive pulmonary sarcoidosis, activation of Th17.1 cells reflects disease activity.