title: Monocyte activation by apoptotic cells removal in systemic lupus erythematosus patients.
abstract: Decreased apoptotic cells (ACs) removal has been described as relevant in systemic lupus erythematosus (SLE) pathogenesis. Binding/phagocytosis of ACs was decreased in SLE patients. Blocking experiments suggested a role for CD36 in ACs clearance in healthy controls, not observed in SLE patients. Binding/phagocytosis of ACs induced the production of IL-6, CXCL8 and CCL22 in patients and controls and IL-1β, TNF-α and CCL3 only in healthy controls. ACs clearance induced an increase in CD80 and a decrease in CD86 expression in healthy controls and atherosclerotic patients. However, SLE patients did not up-regulate CD80 expression. The number and expression of CD36 and CD163 in monocytes was not different between the groups. ACs removal induced a down-regulation of CD36 expression in adherent HLA-DR(+) cells in SLE patients but not healthy controls. The decreased binding/phagocytosis of ACs observed in SLE patients, induces a distinct immune response compared with healthy controls.
authors.affiliation: Universidad de Antioquia, Medellín, Colombia. yascatorce@yahoo.com
authors.forename: Lina M
authors.initials: LM
authors.lastname: Yassin
authors.forename: Mauricio
authors.initials: M
authors.lastname: Rojas
authors.forename: Luis A
authors.initials: LA
authors.lastname: Ramírez
authors.forename: Luis F
authors.initials: LF
authors.lastname: García
authors.forename: Gloria
authors.initials: G
authors.lastname: Vásquez
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000494:pharmacology; D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology / Q000378:metabolism; D017209:Apoptosis / Q000276:immunology*; D050197:Atherosclerosis / Q000276:immunology; D018122:B7-1 Antigen / Q000378:metabolism; D051940:B7-2 Antigen / Q000378:metabolism; D018955:CD36 Antigens / Q000276:immunology / Q000378:metabolism; D019013:CD40 Antigens / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D054422:Chemokine CCL22 / Q000378:metabolism; D054405:Chemokine CCL3 / Q000378:metabolism; D017077:Culture Media, Conditioned / Q000378:metabolism; D005260:Female; D006684:HLA-DR Antigens / Q000378:metabolism; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D010587:Phagocytosis / Q000187:drug effects / Q000276:immunology*; D011956:Receptors, Cell Surface / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult; D000098902:CD163 Antigen
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C111835:CCL2 protein, human; C515482:CCL22 protein, human; C515429:CCL3 protein, human; D000098902:CD163 Antigen; D018955:CD36 Antigens; D019013:CD40 Antigens; C497964:CD86 protein, human; C508606:CXCL8 protein, human; D018932:Chemokine CCL2; D054422:Chemokine CCL22; D054405:Chemokine CCL3; D017077:Culture Media, Conditioned; D006684:HLA-DR Antigens; C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D016209:Interleukin-8; D011956:Receptors, Cell Surface; D014409:Tumor Necrosis Factor-alpha