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• W1581114997 abstract "In this study, messenger RNA (mRNA) expression for novel T described using bioinformatics (5), including the leukotaclymphocyte chemoattractants, leukotactin-1, macrophage inflam- tin-1 (Lkn-1)/CC chemokine ligand (CCL) 15/hemofiltrate CC matory protein (MIP)-3 and MIP-3 was investigated in bronchoal- chemokine-2 (6), macrophage inflammatory protein (MIP)-3/ veolar lavage fluid (BALF) cells from patients with sarcoidosis, a T CCL20/liver and activation-regulated chemokine (7), and cell–mediated disease with typical CD4 lymphocyte alveolitis. Of MIP-3/CCL19/Epstein-Barr virus‐induced molecule 1 ligand these three chemokines, only MIP-3 mRNA was upregulated in chemokine/Exodus 3/CK-11 (7, 8). sarcoidosis, and therefore, protein levels of this chemokine, its phar- The chemokine MIP-3 is expressed especially in lymphoid macologic regulation, and association with disease clinical course tissues, whereas production of MIP-3 is found also in periphwere explored. MIP-3 protein concentrations were elevated in eral blood leukocytes and several fetal tissues (7, 8). ExpresBALF from sarcoid patients compared with control subjects (p sion of Lkn-1 is observed in the liver, intestine, and lung 0.001) and in patients with chest X-ray stage II chemokine protein leukocytes (9). The gene encoding chemokine MIP-3 maps levels were increased compared with stage I (p 0.003). MIP-3 on human chromosome 9, whereas most other CC chemokine protein was associated predominantly with alveolar macrophages genes (including MIP-3 and Lkn-1) are clustered on chroand correlated with BALF lymphocytes and T cell subsets. mRNA" @default.
• W1581114997 created "2016-06-24" @default.
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• W1581114997 date "2003-01-01" @default.
• W1581114997 modified "2023-09-27" @default.
• W1581114997 title "Expression of Macrophage Inflammatory Protein-3/CCL19 in Pulmonary Sarcoidosis" @default.
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• W1581114997 hasPublicationYear "2003" @default.
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