CCL2/CCR2: push/pull for migration

Avvisati, Giuseppe

doi:10.1182/blood-2009-10-250605

Cited by 3 publications

(2 citation statements)

References 6 publications

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“…CXCR4 antagonists are in clinical development for mobilization of stem cells in multiple myeloma and lymphoma patients (phase I and phase II clinical trials). A drawback of disruption of the CXCL12/CXCR4 interaction may be the release of leukaemic cells from the bone marrow into the blood, which may not be desirable in DS (Avvisati, 2009; Burger & Peled, 2009; Horuk, 2009; Xia & Sui, 2009). As multiple chemokine receptors may be involved in the pathogenesis of DS, the use of dual‐chemokine receptor antagonists, such as a CXCR1/CXCR2 antagonists or CCR2/CXCR2 antagonists, may be beneficial therapeutically (Bertini et al , 2004; Walters et al , 2008; Horuk, 2009).…”

Section: Two‐step Model For Pulmonary Infiltration Of Apl Cellsmentioning

confidence: 99%

Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia

Luesink

Jansen

2010

Br J Haematol

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SummaryIn acute promyelocytic leukaemia (APL), differentiation therapy can be complicated by the development of a differentiation syndrome (DS). Pulmonary infiltration of differentiating leukaemic cells is a key event in the development of DS. Several mediators have been identified that may promote migration and extravasation of differentiating APL cells from the bloodstream into the tissue. Adhesion of APL cells to each other and to the endothelium is induced by upregulation of the expression of adhesion molecules and constitutively active b2-integrins during differentiation therapy. The expression of chemokines and their receptors is significantly upregulated as well. Pulmonary chemokine production can trigger transendothelial migration of differentiating APL cells from the bloodstream into the underlying tissue (initiation phase of DS). Massive production of chemokines by infiltrated APL cells can further enhance transendothelial migration of differentiating APL cells, causing an uncontrollable hyperinflammatory reaction in the lung (aggravation phase), which is not efficiently switched-off by corticosteroids.

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Section: Two‐step Model For Pulmonary Infiltration Of Apl Cellsmentioning

confidence: 99%

Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia

Luesink

Jansen

2010

Br J Haematol

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“…Noticeably, the enhanced migration of phagocytes was not caused by nucleotides such as ATP released from apoptotic cells that function as chemoattractants because apyrase, a ATP-diphosphatase, had no effect on cell migration induced by conditioned medium, and the level of ATP was much lower in conditioned medium than in apoptotic supernatants, which is likely due to degradation of ATP by CD39, an ectonucleotidase that catalyzes hydrolysis of triphosphonucleosides to the monophosphonucleoside derivative, expressed in peritoneal macrophages (Figure 3c-e) [27,28]. Ccr2 is the receptor for Mcp-1 and is highly expressed in monocytes [29]. Thus, we next investigated whether the enhanced migration of THP-1 cells to conditioned medium is dependent on Ccr2.…”

Section: Mcp-1 Promotes Phagocyte Chemoattractionmentioning

confidence: 99%

Phagocyte Chemoattraction Is Induced through the Mcp-1–Ccr2 Axis during Efferocytosis

Lee

Kim

Min

et al. 2021

Cells

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Apoptotic cells generated during development and for tissue homeostasis are swiftly and continuously removed by phagocytes via a process called efferocytosis. Efficient efferocytosis can be achieved via transcriptional modulation in phagocytes that have engulfed apoptotic cells. However, such modulation and its effect on efferocytosis are not completely understood. Here, we report that phagocytes are recruited to apoptotic cells being cleared through the Mcp-1–Ccr2 axis, which facilitates clearance of apoptotic cells. We identified Mcp-1 as a modulated transcript using a microarray and found that Mcp-1 secretion was augmented in phagocytes engulfing apoptotic cells. This augmented Mcp-1 secretion was impaired by blocking phagolysosomal degradation of apoptotic cells. Conditioned medium from wild type (WT) phagocytes promoted cell migration, but that from Mcp-1−/− phagocytes did not. In addition, blockade of Ccr2, the receptor for Mcp-1, abrogated cell migration to conditioned medium from phagocytes incubated with apoptotic cells. The intrinsic efferocytosis activity of Mcp-1−/− and Ccr2−/− phagocytes was unaltered, but clearance of apoptotic cells was less efficient in the peritoneum of Mcp-1−/− and Ccr2−/− mice than in that of WT mice because fewer Ccr2-positive phagocytes were recruited. Taken together, our findings demonstrate a mechanism by which not only apoptotic cells but also phagocytes induce chemoattraction to recruit phagocytes to sites where apoptotic cells are cleared for efficient efferocytosis.

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Chemokines in chronic pain: cellular and molecular mechanisms and therapeutic potential

Jiang

Liu

Gao

2020

Pharmacology & Therapeutics

124

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CCL2/CCR2: push/pull for migration

Cited by 3 publications

References 6 publications

Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia

Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia

Phagocyte Chemoattraction Is Induced through the Mcp-1–Ccr2 Axis during Efferocytosis

Chemokines in chronic pain: cellular and molecular mechanisms and therapeutic potential

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