Premium
Increased circulating CD16 + CD14 dim monocytes in a patient with pulmonary alveolar proteinosis
Author(s) -
YOSHIOKA Yasuko,
OHWADA Akihiko,
HARADA Norihiro,
SATOH Naotake,
SAKURABA Shoko,
DAMBARA Takashi,
FUKUCHI Yoshinosuke
Publication year - 2002
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1046/j.1440-1843.2002.00392.x
Subject(s) - medicine , cd16 , pulmonary alveolar proteinosis , cd14 , immunology , granulocyte , granulocyte macrophage colony stimulating factor , myeloid , macrophage , monocyte , macrophage colony stimulating factor , colony stimulating factor , alveolar macrophage , cd64 , pathology , flow cytometry , lung , cytokine , haematopoiesis , immune system , biology , stem cell , in vitro , biochemistry , genetics , cd3 , cd8
Pulmonary alveolar proteinosis (PAP) is characterized by filling of the alveoli with a periodic acid‐Schiff‐positive proteinaceous material. Although the pathogenesis of primary or idiopathic PAP remains unknown, it has been proposed that a deficiency or loss of responsiveness of the monocyte/macrophage lineage to granulocyte–macrophage colony stimulating factor (GM‐CSF) is involved in PAP. Secondary PAP is associated with haematological malignancies, especially in myeloid disorders. Herein, we report on an adult with PAP associated with myelodysplastic syndrome (MDS). The CD16 + CD14 dim monocytes comprise 5–10% of circulating monocytes in healthy volunteers. Flow cytometric analysis of the patient in the present study revealed increased CD16 + CD14 dim monocytes in the peripheral blood. It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M‐CSF) and GM‐CSF. Hence, serum cytokines were analysed in our patient and the concentration of serum GM‐CSF was found to be less than the lower limit of the assay. In addition, serum M‐CSF and granulocyte colony stimulating factor levels were only slightly increased above the normal range. These results suggest that the increase in the CD16 + CD14 dim subpopulation in the circulation of our patient indicates another pathogenetic mechanism for secondary PAP, such as hyperresponsiveness of the monocyte/ macrophage lineage to these cytokines.