RT Journal Article
SR Electronic
T1 Lymphocytes populations in bloods and lungs in patients with auto-immune pulmonary alveolar proteinosis
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP p631
VO 38
IS Suppl 55
A1 Yoshikazu Inoue
A1 Toru Arai
A1 Junji Otsuka
A1 Chikatoshi Sugimoto
A1 Masaki Hirose
A1 Akiko Natsumuro
A1 Yoko Iwaki
A1 Mikiko Nakagawa
A1 Seiji Hayashi
A1 Masaji Okada
YR 2011
UL http://erj.ersjournals.com/content/38/Suppl_55/p631.abstract
AB Background and aim: Pulmonary alveolar proteinosis (PAP) is a rare lung disease which is characterized by pulmonary surfactant accumulation in the lungs, and a subset of PAP which occurs in association with granulocyte/macrophage colony-stimulating factor (GM-CSF) autoantibodies is recommended to call autoimmune pulmonary alveolar proteinosis (APAP) (Inoue Y et al. Am J Respir Crit Care Med. 2008 177:752). We hypothesize that cellular immunity contributed to pathogenesis of APAP. The aim of this study is to know the lymphocytes populations and to clarify the role of lymphocytes in APAP.Subjects and methods: Peripheral bloods (PBMC) and bronchoalveolar lavage fluids (BAL) from 30 patients with APAP, 20 healthy volunteers (HV), and 15 patients with other control diseases (CDs: IIPs, sarcoidosis, etc.) were analyzed. CD3, CD4, CD8, CD19, CD20, CD69, CD3/19, CD3/16, CD3/56, CD16/56, CD4/25, CD14/16, and CD19/69 were measured by flow cytometry.Results: CD3+T cells in PBMC were lower in APAP than HV. CD3+/CD16- in PBMC were significantly lower in APAP than HV. CD4 in PBMC positively correlated with%VC, and negatively correlated with A-aDO2. CD3+T cells in BAL were significantly lower than CDs.Conclusion: We found abnormal T cell populations in APAP, which suggests possible association of T cell immunity on the pathogenesis of APAP.This study was partially supported by the grant-in-aid for scientific research, the grant from Japanese Ministry of Health, Labour, and Welfare, and the grant from National Hospital Organization.