Regulated Expression of Integrins and Other Adhesion Molecules during Differentiation of Monocytes into Macrophages

Prieto, J. Prieto; Eklund, Anders; Patarroyo, Manuel Elkín

doi:10.1006/cimm.1994.1164

Cited by 214 publications

(161 citation statements)

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“…As well, CD11c-CD18 integrins were shown to regulate monocyte adhesion and diapedesis (29). It should be noticed that integrin expression is modulated during monocyte differentiation into macrophages, with an increased expression of CD11c (30). In this regard, the role of collagen on monocyte differentiation through ␣ x ␤ 2 interaction might be important, as suggested by a previous study on dendritic cells (31).…”

Section: Discussionmentioning

confidence: 73%

Human Blood Monocytes Interact with Type I Collagen Through αxβ2 Integrin (CD11c-CD18, gp150-95)

Garnotel

Rittié

Poitevin

et al. 2000

The Journal of Immunology

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Section: Discussionmentioning

confidence: 73%

Human Blood Monocytes Interact with Type I Collagen Through αxβ2 Integrin (CD11c-CD18, gp150-95)

Garnotel

Rittié

Poitevin

et al. 2000

The Journal of Immunology

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“…In contrast, the expression of costimulatory molecules (CD80, CD86 and CD40) was higher in AM, in the three groups studied. These differences reflect the process of maturation of PBM into AM [25,30,31]. …”

Section: Comparison Of Pbm and Am Surface Phenotypementioning

confidence: 99%

Phenotypic characterisation of alveolar macrophages and peripheral blood monocytes in COPD

Pons¹

2005

Eur Respir J

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Alveolar macrophages (AM) participate actively in the inflammatory response that characterises chronic obstructive pulmonary disease (COPD). The present study investigated potential changes in AM phenotypes in patients with COPD.Using flow cytometry, the surface expression of receptors implicated in phagocytosis (CD44, CD36, CD51, CD61, CD14), antigen-presenting capacity (human leukocyte antigen (HLA)-DR), costimulatory molecules (CD80, CD86, CD40) and complement receptor type 3 were assessed in AM from 18 patients with COPD, 14 smokers with normal lung function and nine nonsmokers.When compared to smokers with normal lung function and nonsmokers, the surface expression of HLA-DR and CD80 was lower in AM of patients with COPD. In addition, these patients had a higher percentage of AM with a low level surface expression of CD44. There did not appear to be any difference in the other receptors studied in AM between the three groups. The expression of all these receptors in peripheral blood monocytes also did not differ between groups.In conclusion, these observations suggest that the cell-mediated immune function of alveolar macrophages can be reduced in chronic obstructive pulmonary disease, and that this is a local rather than a systemic event.

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“…In monocytes/macrophages, CD36 expression is up regulated by adhesion (Prieto, Eklund, & Patarroyo, 1994,Huh, Lo, Yesner, & Silverstein, 1995, differentiation (Huh, Pearce, Yesner, Schindler, & Silverstein, 1996), certain nuclear hormone receptors and cytokines. For example, CD36 is up regulated in response to the cytokine IL-4 and oxLDL by a common signaling pathway involving protein kinase C and PPAR-γ .…”

Section: Cd36 Regulationmentioning

confidence: 99%

CD36: Implications in cardiovascular disease

Febbraio

Silverstein

2007

The International Journal of Biochemistry & Cell Biology

215

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CD36 is a broadly expressed membrane glycoprotein that acts as a facilitator of fatty acid uptake, a signaling molecule, and a receptor for a wide range of ligands, including apoptotic cells, modified forms of low density lipoprotein, thrombospondins, fibrillar beta-amyloid, components of gram positive bacterial walls and malaria infected erythrocytes. CD36 expression on macrophages, dendritic and endothelial cells, and in tissues including muscle, heart, and fat, suggest diverse roles, and indeed, this is truly a multifunctional receptor involved in both homeostatic and pathologic conditions. Despite an impressive increase in our knowledge of CD36 functions, in depth understanding of the mechanistic aspects of this protein remains elusive. This review focuses on CD36 in cardiovascular disease-what we know, and what we have yet to learn.

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Regulated Expression of Integrins and Other Adhesion Molecules during Differentiation of Monocytes into Macrophages

Cited by 214 publications

References 0 publications

Human Blood Monocytes Interact with Type I Collagen Through αxβ2 Integrin (CD11c-CD18, gp150-95)

Human Blood Monocytes Interact with Type I Collagen Through αxβ2 Integrin (CD11c-CD18, gp150-95)

Phenotypic characterisation of alveolar macrophages and peripheral blood monocytes in COPD

CD36: Implications in cardiovascular disease

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