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Expression of Macrophage Inflammatory Protein-3ß/CCL19 in Pulmonary Sarcoidosis

Departments of Immunology and Respiratory Medicine, Palacky University, Olomouc, Czech Republic; and Interstitial Lung Disease Unit, Royal Brompton Hospital, London, United Kingdom

Correspondence and requests for reprints should be addressed to Dr. Martin Petrek, M.D., Department of Immunology, Palacky University, I. P. Pavlova str. 6, Olomouc CZ-775 20, Czech Republic. E-mail: martinpe{at}email.cz

In this study, messenger RNA (mRNA) expression for novel T lymphocyte chemoattractants, leukotactin-1, macrophage inflammatory protein (MIP)-3 and MIP-3ß was investigated in bronchoalveolar lavage fluid (BALF) cells from patients with sarcoidosis, a T cell–mediated disease with typical CD4+ lymphocyte alveolitis. Of these three chemokines, only MIP-3ß mRNA was upregulated in sarcoidosis, and therefore, protein levels of this chemokine, its pharmacologic regulation, and association with disease clinical course were explored. MIP-3ß protein concentrations were elevated in BALF from sarcoid patients compared with control subjects (p = 0.001) and in patients with chest X-ray stage II chemokine protein levels were increased compared with stage I (p = 0.003). MIP-3ß protein was associated predominantly with alveolar macrophages and correlated with BALF lymphocytes and T cell subsets. mRNA expression for the MIP-3ß receptor, CC chemokine receptor 7, was increased in sarcoidosis and correlated with MIP-3ß protein levels. MIP-3ß mRNA and protein expression in BALF cells was suppressed by dexamethasone and cyclosporine A in vitro. In conclusion, MIP-3ß is implicated in T lymphocyte recruitment in sarcoidosis, is associated with disease progression, and is downregulated by drugs used for sarcoidosis treatment. This novel chemokine, therefore, represents a candidate for studies of sarcoidosis pathobiologic mechanisms.

Key Words: chemokine • leukotactin-1 • CC chemokine receptor 7 • dexamethasone • cyclosporine A

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