Literature DB >> 17673663

Monitoring of blood vessels and tissues by a population of monocytes with patrolling behavior.

Cedric Auffray1, Darin Fogg, Meriem Garfa, Gaelle Elain, Olivier Join-Lambert, Samer Kayal, Sabine Sarnacki, Ana Cumano, Gregoire Lauvau, Frederic Geissmann.   

Abstract

The cellular immune response to tissue damage and infection requires the recruitment of blood leukocytes. This process is mediated through a classical multistep mechanism, which involves transient rolling on the endothelium and recognition of inflammation followed by extravasation. We have shown, by direct examination of blood monocyte functions in vivo, that a subset of monocytes patrols healthy tissues through long-range crawling on the resting endothelium. This patrolling behavior depended on the integrin LFA-1 and the chemokine receptor CX(3)CR1 and was required for rapid tissue invasion at the site of an infection by this "resident" monocyte population, which initiated an early immune response and differentiated into macrophages.

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Year:  2007        PMID: 17673663     DOI: 10.1126/science.1142883

Source DB:  PubMed          Journal:  Science        ISSN: 0036-8075            Impact factor:   47.728


  770 in total

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2.  A chemotactic gradient sequestered on endothelial heparan sulfate induces directional intraluminal crawling of neutrophils.

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4.  CX3CR1+ lung mononuclear phagocytes spatially confined to the interstitium produce TNF-α and IL-6 and promote cigarette smoke-induced emphysema.

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Review 6.  Contributions of monocytes to nervous system disorders.

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7.  Genetic disruption of fractalkine signaling leads to enhanced loss of cochlear afferents following ototoxic or acoustic injury.

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Review 9.  From proliferation to proliferation: monocyte lineage comes full circle.

Authors:  Filip K Swirski; Ingo Hilgendorf; Clinton S Robbins
Journal:  Semin Immunopathol       Date:  2014-01-17       Impact factor: 9.623

10.  Ribosomal protein L13a deficiency in macrophages promotes atherosclerosis by limiting translation control-dependent retardation of inflammation.

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