Affiliation:
1. Third Department of Internal Medicine, Kagoshima University Faculty of Medicine, Kagoshima, Japan
2. Department of Respiratory Medicine, National Minami-kyushu Hospital, Kagoshima Japan
Abstract
SUMMARY
Human T lymphotrophic virus type-I (HTLV-I), a human retrovirus, infects CD4+ lymphocytes and is thought to modify their function and a possible association with pulmonary diseases has also been suggested. However, little is known about the influence of HTLV-I on diffuse pan-bronchiolitis (DPB), a chronic inflammatory lung disease with infiltration of lymphocytes and hyperplasia of the bronchus-associated lymphoid tissue. In this study, 35 DPB patients with and without HTLV-I infection were examined. HTLV-I positive DPB patients were likely to have a larger affected area with lower FEV1. The CD3+/CD25+ lymphocyte percentage was significantly higher in the BALF of HTLV-I positive patients than in negative patients. MIP-1α, IP-10 and levels in BALF were also significantly higher in HTLV-I positive patients than in negative patients. The levels of MCP-1 and IL-8 were not significantly different. In HTLV-I positive patients, the MIP-1α and IP-10 levels showed a significant positive correlation with the percentage of CD3+/CD25 lymphocytes. BALF cells of all HTLV-I positive DPB patients showed expression of p40tax mRNA. We suggest that HTLV-I infection may modify DPB pathogenesis via activation of T cells. We also found that the frequency of ATL development in HTLV-I positive DPB patients was significantly higher than in all HTLV-I positive patients (OR = 8·22, 95% CI = 2·61–25·9, P < 0·01). The levels of TGF-β in patients who developed ATL were significantly lower than in patients who did not develop ATL. Sensitivity and specificity were 80% and 85·7%, respectively (cut-off = 20 pg/ml). We also propose that these features should be taken into consideration in the treatment of DPB in HTLV-I infected individuals.
Publisher
Oxford University Press (OUP)
Subject
Immunology,Immunology and Allergy
Cited by
10 articles.
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