Previously unreported CD8+CD28− and CD8+CD28+ T-cell subsets occur in healthy individuals and expand in patients suffering from autoimmune disease. Here we studied, for the first time, the expression of CD8+CD28+, CD8+CD28−, and CD8+CD56+ subpopulations in induced sputum from asthmatics. Using sputum samples, purified CD8+ T cells were stained for surface antigen CD28, CD56, FITC-conjugated anti-perforin, and anti-IFN-γ. Cytotoxic activity was evaluated in a chromium releasing test. Induced sputum CD8+CD28− T cells were found to be more expanded and expressed low levels of IFN-γ in severe asthmatics than mild asthma and age-matched healthy controls. The predominance of CD8+CD28− T cells can be in part explained by the expansion of CD8+CD56+. CD8+CD28− T cells from severe asthmatics produced high intracytoplasmic perforin and exerted a potent cytotoxic activity. Considering their phenotyping and functional properties, the CD8+CD28− T-cell subset may constitute an intermediate phenotype in the process of CD8+ T-cell differentiation of effector-type cells in severe asthmatics. Functional studies showed that CD8+CD28− T cells had cytotoxic function.
Castleman's disease (CD) is an uncommon, mainly benign, lymphoproliferative disorder of unknown etiology, mostly involving the mediastinum. Parenchymal lung involvement of the disease is exceedingly rare. We describe a case of CD in a 23-year-old woman with a 4-year history of recurring dyspnea and nonproductive cough, whose chest X-ray showed an abnormal shadow of the right hilum. Chest computed tomography confirmed the presence of a tissue-density mass of the right lower lobe, demonstrating poor contrast enhancement, associated with multiple laterotracheal and mediastinal lymphadenopathies. The patient underwent curative surgery, revealing a right hilar compressive mass, with an intrafissural development between the superior and middle lobes. Pneumonectomy was performed due to profuse bleeding. This case of CD is particular because of its unusual intrapulmonary location and its intrafissural development. Poor contrast enhancement is atypical in CD.
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