Junction Adhesion Molecule Is a Receptor for Reovirus

Barton, Erik S.; Forrest, J. Craig; Connolly, Jodi L.; Chappell, James D.; Liu, Yuan; Schnell, Frederick J.; Nusrat, Asma; Parkos, Charles A.; Dermody, Terence S.

doi:10.1016/s0092-8674(01)00231-8

Cited by 593 publications

(562 citation statements)

References 58 publications

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“…Polyclonal Ab 177 was raised in rabbits against the extracellular domain of PECAM (Covance) and column purified on protein A-Sepharose (Amersham Biosciences). Anti-junctional adhesion molecule (JAM)-A mAb (clone 1H2A9) was generated as described previously (27). Fab and F(abЈ) 2 were cut from hec2 IgG1 using immobilized ficin (Pierce) according to the manufacturer's protocol and purified using protein G column chromatography.…”

Section: Antibodiesmentioning

confidence: 99%

CD99 Is a Key Mediator of the Transendothelial Migration of Neutrophils

Lou

Alcaide

Luscinskas

et al. 2007

The Journal of Immunology

157

145

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Transendothelial migration of leukocytes is a critical event for inflammation, but the molecular regulation of this event is only beginning to be understood. PECAM (CD31) is a major mediator of monocyte and neutrophil transmigration, and CD99 was recently defined as a second mediator of the transmigration of monocytes. Expression of CD99 on the surface of circulating polymorphonuclear cells (PMN) is low compared with expression of CD99 on monocytes or expression of PECAM on PMN. We demonstrate here that, despite low expression of CD99, Fab of Abs against CD99 blocked over 80% of human neutrophils from transmigrating across HUVEC monolayers in an in vitro model of inflammation. Blocking CD99 on either the neutrophil or endothelial cell side resulted in a quantitatively equivalent block, suggesting a homophilic interaction between CD99 on the neutrophil and CD99 on the endothelial cell. Blocking CD99 and PECAM together resulted in additive effects, suggesting the two molecules work at distinct steps. Confocal microscopy confirmed that CD99-blocked neutrophils lodged in endothelial cell junctions at locations distal to PECAM-blocked neutrophils. The CD99-blocked PMN exhibited dynamic lateral movement within endothelial cell junctions, indicating that only the diapedesis step was blocked by interference with CD99. Anti-CD99 mAb also blocked PMN transmigration in a second in vitro model that incorporated shear stress. Taken together, the evidence demonstrates that PECAM and CD99 regulate distinct, sequential steps in the transendothelial migration of neutrophils during inflammation.

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Section: Antibodiesmentioning

confidence: 99%

CD99 Is a Key Mediator of the Transendothelial Migration of Neutrophils

Lou

Alcaide

Luscinskas

et al. 2007

The Journal of Immunology

157

145

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“…Although speculative, the function of VCBPs might be to recognize determinants on various pathogens. There is considerable precedent for IgSF-related viral receptors, including those for poliovirus (poliovirus receptor) 116 , reovirus (junctional adhesion molecule, JAM) 117 , HIV (CD4) 118 , mouse hepatitis virus (CEA-related cell-adhesion molecule 1, CEACAM1) 119 , measles virus (signalling lymphocytic activation molecule, SLAM) 120 and others. Other potential functions for VCBPs include binding to fungal or bacterial surfaces, direct opsonization, and self-and non-self-recognition 3,7 .…”

Section: Vcbps In Protochordatesmentioning

confidence: 99%

Reconstructing immune phylogeny: new perspectives

2005

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Numerous studies of the mammalian immune system have begun to uncover profound interrelationships, as well as fundamental differences, between the adaptive and innate systems of immune recognition. Coincident with these investigations, the increasing experimental accessibility of non-mammalian jawed vertebrates, jawless vertebrates, protochordates and invertebrates has provided intriguing new information regarding the likely patterns of emergence of immune-related molecules during metazoan phylogeny, as well as the evolution of alternative mechanisms for receptor diversification. Such findings blur traditional distinctions between adaptive and innate immunity and emphasize that, throughout evolution, the immune system has used a remarkably extensive variety of solutions to meet fundamentally similar requirements for host protection.The evolutionary development of the METAZOANS was associated with the diversification of a wide range of specialized cell-surface molecules that mediate key metabolic processes, as well as provide crucial contact interfaces and carry out a broad range of other essential functions. It is not unexpected that some of these molecules also came to function as barriers to pathogenic invasion and, in doing so, began to carry out dedicated innate immune protective functions. Whereas the simplest form of protection, barrier formation, is essentially mechanical in nature, relentless pressure from genetic variation in pathogens probably drove the evolution of such innate immune protective molecules towards diversification and, in parallel, towards integration of signalling pathways to regulate cellular responses to external stimulation. However, despite the sophistication that such innate immune mediators achieved over time, their biological complexity, by definition, would be limited by genome space, so with increasing complexity of body plan and/or increasing pathogen sophistication, they could be overwhelmed. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptMore than 500 million years ago, a TRANSPOSITION event, probably involving a recombinationactivating gene (RAG)-bearing element, might have given rise to the predecessors of the rearranging antigen-binding receptors of the jawed vertebrates, which encompass the vertebrate radiations that extend from the cartilaginous fish through to humans. This is considered the defining point in the emergence of RAG-mediated (conventional) adaptive immunity 1,2 , which has evolved to create a mechanism for deriving almost limitless variation from very few genes. Studies in traditional and non-traditional animal models, such as sharks, bony fish and birds, have brought this event and its ramifications for host defence into sharper focus. We can now predict much about how these rearranging antigenbinding receptors probably arose, what alternative pathways of immune-receptor gene evolution have occurred, what relationships exist between B-and T-cell-mediated immunity and natural killer (NK)-cell function, how complex immune ...

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“…Tardieu et al speculated that the age-dependent resistance to reovirus appears to be related to an intrinsic resistance to viral replication by cells, but had no relation with modification or loss of viral receptors [18]. In contrast, Barton et al were of the opinion that mouse JAM-A is highly expressed at birth, after which its expression declines, and this is responsible for the higher resistance in adults [2,6]. However, JAM-A expression during development has not been clearly examined in the murine model.…”

Section: Discussionmentioning

confidence: 99%

“…Reoviruses infect most mammalian species [1], and the receptor for reovirus in humans and other mammals is junction adhesion molecule A (JAM-A) [2,3], a member of the immunoglobulin superfamily. JAM-A regulates the formation of intercellular tight junctions [4] and is involved in platelet activation, leukocyte transmigration and angiogenesis [5,6].…”

Section: Introductionmentioning

confidence: 99%

Cloning and preliminary functional studies of the JAM-A gene in grass carp (Ctenopharyngodon idellus)

Huang

et al. 2013

Fish & Shellfish Immunology

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Junction Adhesion Molecule Is a Receptor for Reovirus

Cited by 593 publications

References 58 publications

CD99 Is a Key Mediator of the Transendothelial Migration of Neutrophils

CD99 Is a Key Mediator of the Transendothelial Migration of Neutrophils

Reconstructing immune phylogeny: new perspectives

Cloning and preliminary functional studies of the JAM-A gene in grass carp (Ctenopharyngodon idellus)

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