CD100 and plexins B2 and B1 mediate monocyte-endothelial cell adhesion and might take part in atherogenesis.
Leukocyte migration is essential for the function of the immune system. Their recruitment from the vessels to the tissues involves sequential molecular interactions between leukocytes and endothelial cells (ECs). Many adhesion molecules involved in this process have already been described. However, additional molecules may be important in this interaction, and here we explore the potential role for CD100 and plexins in monocyte-EC binding. CD100 was shown to be involved in platelet-endothelial cell interaction, an important step in atherogenesis and thrombus formation. In a recent work we have described CD100 expression in monocytes and in macrophages and foam cells of human atherosclerotic plaques. In the present work, we have identified plexin B2 as a putative CD100 receptor in these cells. We have detected CD100 expression in the endothelium as well as in in vitro cultured endothelial cells. Blocking of CD100, plexin B1 and/or B2 in adhesion experiments have shown that both CD100 and plexins act as adhesion molecules involved in monocyte-endothelial cell binding. This effect may be mediated by CD100 expressed in both cell types, probably coupled to the receptors endothelial plexin B1 and monocytic plexin B2. These results can bring new insights about a possible biological activity of CD100 in monocyte adhesion and atherosclerosis, as well as a future candidate for targeting therapeutics.
Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, SP, Brazil; Clinical Immunology and Allergy, Department of Clinical Medicine, University of São Paulo Medical School-HC-FMUSP, São Paulo, SP, Brazil.
Maria Carolina A
MC
Luque
Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, SP, Brazil.
Paulo S
PS
Gutierrez
Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, SP, Brazil.
Victor
V
Debbas
Heart Institute of São Paulo (InCor), HC-FMUSP, São Paulo, SP, Brazil; Clinical Immunology and Allergy, Department of Clinical Medicine, University of São Paulo Medical School-HC-FMUSP, São Paulo, SP, Brazil; Institute for Investigation in Immunology - INCT - National Institute of Science and Technology, São Paulo, SP, Brazil.
Jorge
J
Kalil
Department of Parasitology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil. Electronic address: bstolf@usp.br.
Beatriz S
BS
Stolf
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism*; D050197:Atherosclerosis / Q000378:metabolism* / Q000473:pathology*; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002454:Cell Differentiation; D002478:Cells, Cultured; D005487:Foam Cells / Q000378:metabolism; D005786:Gene Expression Regulation; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D051379:Mice; D009000:Monocytes / Q000166:cytology*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism*; D039961:Semaphorins / Q000235:genetics / Q000378:metabolism*
D015703:Antigens, CD; C093224:CD100 antigen; D015815:Cell Adhesion Molecules; D009419:Nerve Tissue Proteins; C492119:PLXNB1 protein, human; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D039961:Semaphorins; C091529:plexin
Atherosclerosis; Monocyte adhesion; Plexins; SEMA4D