title: Increased expression of CCL4/MIP-1β in CD8+ cells and CD4+ cells in sarcoidosis.
abstract: Sarcoidosis is a granulomatous disease with an increased accumulation of T cells in lungs as a result of on-site proliferation and chemotaxis induced by chemokines. It has already been demonstrated that CCL3-5 levels were increased in BAL fluid of sarcoidosis patients. To analyze the expression of CCL3-5 chemokines by T-cell subtypes (CD4+, CD8+, Th1, Th2, Tc1 or Tc2) in the lungs of sarcoidosis patients, fifteen untreated sarcoidosis patients and eighteen control subjects were enrolled in this study. CD4+ and CD8+ cells were isolated from BAL fluid by positive magnetic selection. The expression of CCL3-5 and other cytokines in CD4+ and CD8+ cells were measured by flow cytometry. The percentage of CD4+ or CD8+ cells expressing CCL4 were significantly higher in sarcoidosis patients (22.3&#x0025; and 58.1&#x0025;) compared to those seen in healthy subjects (11.1&#x0025; and 16.5&#x0025;, P = 0.04 and P = 0.02, respectively). In addition, the expression of CCL3, CCL4 and CCL5 was significantly elevated in CD8+ cells (8.9&#x0025;, 58.1&#x0025; and 2.1&#x0025;) compared to CD4+ cells (2.1&#x0025;, 22.3&#x0025; and 0.7&#x0025;; P = 0.04, P = 0.009 and P = 0.04, respectively), whereas CCL4 was expressed by significantly more Tc1 than Th1 cells in sarcoidosis patients (P = 0.006). Our study shows the possible role of CD8+ cells and CD4+ cells in recruiting T cells to the site of inflammation in sarcoidosis through the release of CCL4, either alone or together with Th1/Tc1-associated cytokines.
authors.affiliation: Department of Pneumonology, Medical University of Silesia, Katowice, Poland.
authors.forename: A
authors.initials: A
authors.lastname: Barczyk
authors.affiliation: Department of Cosmetology, Institute of Aesthetic Medicine, Medical University of Silesia, Katowice, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Pierzchała
authors.affiliation: Department of Clinical and Experimental Medicine, Respiratory Disease Section, University of Ferrara, Ferrara, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Caramori
authors.affiliation: Department of Pneumonology, Medical University of Silesia, Katowice, Poland.
authors.forename: E
authors.initials: E
authors.lastname: Sozańska
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D018791:CD4 Lymphocyte Count; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016022:Case-Control Studies; D002450:Cell Communication; D054405:Chemokine CCL3 / Q000032:analysis; D054407:Chemokine CCL4 / Q000032:analysis*; D018946:Chemokine CCL5 / Q000032:analysis; D002634:Chemotaxis, Leukocyte; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008168:Lung / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D017565:Sarcoidosis, Pulmonary / Q000276:immunology* / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; C515429:CCL3 protein, human; C066507:CCL4 protein, human; C483024:CCL5 protein, human; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5