Regulated Expression of the Pathogen Receptor Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin in THP-1 Human Leukemic Cells, Monocytes, and Macrophages

Puig‐Kröger, Amaya; Serrano‐Gómez, Diego; Caparrós, Esther; Domínguez-Soto, Ángeles; Relloso, Miguel; Colmenares, Marı́a; Martínez-Muñoz, Laura; Longo, Natividad; Sánchez-Sánchez, Noelia; Rincón, Mercedes; Rivas, Luís; Sánchez‐Mateos, Paloma; Fernández‐Ruiz, Elena; Corbí, Ángel L.

doi:10.1074/jbc.m311516200

Cited by 94 publications

(119 citation statements)

References 36 publications

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“…This effect is also seen in THP-1 cells driven along their alternative differentiation pathway (31). The differential expression of CD36 in CAM and AAM might be of relevance, especially considering that CD36 has important roles in foam cell formation by mediating oxidized low-density lipoprotein uptake (1) and in monocyte proliferation and recruitment through its interaction with ␤-amyloid (2).…”

Section: Discussionmentioning

confidence: 99%

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

Puig‐Kröger

Domínguez-Soto

Martínez-Muñoz

et al. 2006

The Journal of Immunology

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CD36 is a member of the scavenger receptor type B family implicated in the binding of lipoproteins, phosphatidylserine, thrombospondin-1, and the uptake of long-chain fatty acids. On mononuclear phagocytes, recognition of apoptotic cells by CD36 contributes to peripheral tolerance and prevention of autoimmunity by impairing dendritic cell (DC) maturation. Besides, CD36 acts as a coreceptor with TLR2/6 for sensing microbial diacylglycerides, and its deficiency leads to increased susceptibility to Staphylococcus aureus infections. The RUNX3 transcription factor participates in reprogramming DC transcription after pathogen recognition, and its defective expression leads to abnormally accelerated DC maturation. We present evidence that CD36 expression is negatively regulated by the RUNX3 transcription factor during myeloid cell differentiation and activation. In molecular terms, RUNX3 impairs the activity of the proximal regulatory region of the CD36 gene in myeloid cells through in vitro recognition of two functional RUNX-binding elements. Moreover, RUNX3 occupies the CD36 gene proximal regulatory region in vivo, and its overexpression in myeloid cells results in drastically diminished CD36 expression. The down-regulation of CD36 expression by RUNX3 implies that this transcription factor could impair harmful autoimmune responses by contributing to the loss of pathogen- and apoptotic cell-recognition capabilities by mature DCs.

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Section: Discussionmentioning

confidence: 99%

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

Puig‐Kröger

Domínguez-Soto

Martínez-Muñoz

et al. 2006

The Journal of Immunology

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“…Toward this end, the LPS from lgtB Ϫ pagL ϩ and galE Ϫ lpxL1 Ϫ meningococci were assayed for cytokine induction in the human monocytic cell line MM6. Because MM6 cells do not express DC-SIGN (36), in contrast to human DC cells, they are not expected to react differently to LPS carrying an lgtB oligosaccharide truncation. In fact, the presence of lgtB Ϫ or galE Ϫ oligosaccharide mutations does not influence cytokine response in MM6 cells to hexaacylated LPS (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Lipopolysaccharide Engineering in Neisseria meningitidis

Pupo

Hamstra

Meiring

et al. 2014

Journal of Biological Chemistry

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“…Detection of PU.1 was carried out using specific affinity-purified rabbit polyclonal antibody (sc-352; Santa Cruz Biotechnology, Inc., Santa Cruz, CA). DC-SIGN was detected using a polyclonal antiserum raised against the 23-residue repeats within the neck region of the molecule (10).…”

Section: Methodsmentioning

confidence: 99%

“…After nucleofection, cells were maintained in culture for 24 h, and one-fifth of the cells were lysed and subjected to Western blot for detection of PU.1, DC-SIGN, or ␤-actin as control. Total RNA was isolated from the rest of nucleofected cells and subjected to reverse transcription-PCR for detection of DC-SIGN and glyceraldehyde-3-phosphate dehydrogenase RNA, as previously described (10). 2 g of RNA from cells transfected with either PU.1-specific or control siRNA was reverse transcribed, and 5 l of the resulting cDNA was subjected to PCR with oligonucleotides CD209sense (5Ј-GGGAATTCAGAGTGGGGTGACATGAGTGAC-3Ј) and CD209a-ntisense (5Ј-CCCCAAGCTTGTGAAGTTCTGCTACGCAGGAG-3Ј) to amplify the whole coding region of DC-SIGN.…”

Section: Methodsmentioning

confidence: 99%

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PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

Domínguez-Soto¹,

Puig‐Kröger²,

Vega

et al. 2005

Journal of Biological Chemistry

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Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) is a cell surface C-type lectin expressed on myeloid dendritic cells and certain tissue macrophages, which mediates antigen capture for processing and presentation and participates in intercellular interactions with naive T lymphocytes or endothelial cells. In their strategy to evade immunosurveillance, numerous pathogenic microorganisms, including human immunodeficiency virus and Mycobacterium, bind to DC-SIGN in order to gain access to dendritic cells. We present evidence that PU.1 dictates the basal and cell-specific activity of DC-SIGN gene-regulatory region through in vivo occupancy of two functional Ets elements, whose integrity is required for PU.1 responsiveness and for the cooperative actions of PU.1 and other transcription factors (Myb, RUNX) on the DC-SIGN gene proximal regulatory region. In addition, protein analysis and gene profiling experiments indicate that DC-SIGN and PU.1 are coordinately expressed upon classical and alternative macrophage activation and during dendritic cell maturation. Moreover, small interfering RNA-mediated reduction of PU.1 expression results in diminished DC-SIGN cellular levels. Altogether, these results indicate that PU.1 is involved in the myeloid-specific expression of DC-SIGN in myeloid cells, a contribution that can be framed within the role that PU.1 has on the acquisition of the antigen uptake molecular repertoire by dendritic cells and macrophages.

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Regulated Expression of the Pathogen Receptor Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin in THP-1 Human Leukemic Cells, Monocytes, and Macrophages

Abstract: Dendritic cell-specific ICAM-3-grabbing nonintegrin (DC-SIGN) is a type II C-type lectin that functions as an

Cited by 94 publications

References 36 publications

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

RUNX3 Negatively Regulates CD36 Expression in Myeloid Cell Lines

Lipopolysaccharide Engineering in Neisseria meningitidis

PU.1 Regulates the Tissue-specific Expression of Dendritic Cell-specific Intercellular Adhesion Molecule (ICAM)-3-grabbing Nonintegrin

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