title: Control of dendritic cell differentiation by angiotensin II.
abstract: Here we analyze the role of the angiotensinergic system in the differentiation of dendritic cells (DC). We found that human monocytes produce angiotensin II (AII) and express AT1 and AT2 receptors for AII. DC differentiated from human monocytes in the presence of AT1 receptor antagonists losartan or candesartan show very low levels of CD1a expression and poor endocytic and allostimulatory activities. By contrast, DC differentiation in the presence of either the AT2 receptor antagonist PD 123319 or exogenous AII results in the development of nonadherent cells with CD1a expression and endocytic and allostimulatory activities higher than control DC. Similar contrasting effects were observed in mouse DC obtained from bone marrow cultures supplemented with granulocyte-monocyte colony-stimulating factor. DC differentiated in the presence of the AT1 receptor antagonist losartan express lower levels of CD11c, CD40, and Ia and display a lower ability to endocyte horseradish peroxidase (HRP) and to induce antibody responses in vivo, compared with controls. By contrast, DC differentiation in the presence of either the AT2 receptor antagonist PD 123319 or exogenous AII results in cells with high levels of CD11c, CD40, and Ia, as well as high ability to endocyte HRP and to induce antibody responses in vivo. Our results support the notion that the differentiation of DC is regulated by AII.
authors.affiliation: Laboratory of Immunology, Institute of Hematologic Research, National Academy of Medicine, Buenos Aires, Argentina.
authors.forename: Karen A
authors.initials: KA
authors.lastname: Nahmod
authors.forename: Monica E
authors.initials: ME
authors.lastname: Vermeulen
authors.forename: Silvina
authors.initials: S
authors.lastname: Raiden
authors.forename: Gabriela
authors.initials: G
authors.lastname: Salamone
authors.forename: Romina
authors.initials: R
authors.lastname: Gamberale
authors.forename: Paula
authors.initials: P
authors.lastname: Fernández-Calotti
authors.forename: Azucena
authors.initials: A
authors.lastname: Alvarez
authors.forename: Victor
authors.initials: V
authors.lastname: Nahmod
authors.forename: Mirta
authors.initials: M
authors.lastname: Giordano
authors.forename: Jorge R
authors.initials: JR
authors.lastname: Geffner
mesh_terms: D000804:Angiotensin II / Q000378:metabolism / Q000502:physiology*; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D000906:Antibodies / Q000378:metabolism; D001562:Benzimidazoles / Q000494:pharmacology; D001713:Biphenyl Compounds / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D004705:Endocytosis; D006412:Hematopoietic Stem Cells / Q000502:physiology; D006801:Humans; D000077405:Irbesartan; D019808:Losartan / Q000494:pharmacology; D008213:Lymphocyte Activation; D051379:Mice; D008954:Models, Biological; D009000:Monocytes; D010641:Phenotype; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000378:metabolism; D013777:Tetrazoles / Q000494:pharmacology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000906:Antibodies; D001562:Benzimidazoles; D001713:Biphenyl Compounds; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D013777:Tetrazoles; D000804:Angiotensin II; D000077405:Irbesartan; D019808:Losartan; C081643:candesartan