Plasticity in leukocyte migration during haematopoiesis and inflammation.

IF 1.8 3区 生物学 Q4 CELL BIOLOGY
C Villella, M Ciccioli, I M Anton, Y Calle
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引用次数: 0

Abstract

Under normal physiological conditions, leukocytes and other tissue resident immune cells have been shown to migrate using the mesenchymal (integrin/adhesion dependent) and/or ameboid (integrin/adhesion independent) modes of migration. The objective of this manuscript is to provide a comprehensive literature review that illustrates how leukocytes display high levels of plasticity shifting between ameboid to mesenchymal modes of migration during haematopoiesis and the inflammatory response. This plasticity is shaped by the reciprocal regulation between the pattern of gene expression associated with their haematopoietic lineage or the leukocyte activation status, and the response to the physicochemical and topological characteristics of the surrounding tissue. The use of some common elements from the F-actin polymerising and actomyosin machinery in both modes of migration may facilitate the high capacity of leukocytes to alternate between the two migration modes while navigating a highly heterogenous landscape of physicochemical cues in their anatomical journey. We discuss this paradigm using detailed examples of specific leukocyte populations such as dendritic cells, macrophages and lymphocytes. We propose that cell adhesions involved in leukocyte migration represent signalling hubs where differentiation and physicochemical cues converge. These molecular complexes then generate signalling outputs that coordinate leukocyte expansion, differentiation, and optimal patterns of cell migration during haematopoiesis and leukocyte recruitment to inflammation sites.

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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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