The Inducible CXCR3 Ligands Control Plasmacytoid Dendritic Cell Responsiveness to the Constitutive Chemokine Stromal Cell–derived Factor 1 (SDF-1)/CXCL12

Vanbervliet, Béatrice; Bendriss‐Vermare, Nathalie; Massacrier, Catherine; Homey, Bernhard; Bouteiller, Odette de; Brière, Francine; Trinchieri, Giorgio; Caux, Christophe

doi:10.1084/jem.20020437

Cited by 221 publications

(197 citation statements)

References 30 publications

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“…However, with the exception of CXCR4, these receptors are apparently nonfunctional in transwell-based chemotaxis assays [35,42,43]. Although unable to directly induce PDCs migration, CXCR3 ligands increase the chemotactic response to CXCL12 [42,43].…”

Section: Molecules Involved In Pdcs Traffickingmentioning

confidence: 99%

Trafficking properties of plasmacytoid dendritic cells in health and disease

Sozzani

Vermi

Prete

et al. 2010

Trends in Immunology

138

144

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Section: Molecules Involved In Pdcs Traffickingmentioning

confidence: 99%

Trafficking properties of plasmacytoid dendritic cells in health and disease

Sozzani

Vermi

Prete

et al. 2010

Trends in Immunology

138

144

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“…Only recently, a broad phenomenon known as ''chemokine synergism'' has been identified [2][3][4][5][6][7][8][9][10]. Cells expressing two or more chemokine receptors, in the presence of the selective agonists, can amplify their response [2][3][4][5][6]11].…”

Section: Introductionmentioning

confidence: 99%

Synergy‐inducing chemokines enhance CCR2 ligand activities on monocytes

Kuscher¹,

Danelon²,

Paoletti³

et al. 2009

Eur J Immunol

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The migration of monocytes to sites of inflammation is largely determined by their response to chemokines. Although the chemokine specificities and expression patterns of chemokine receptors are well defined, it is still a matter of debate how cells integrate the messages provided by different chemokines that are concomitantly produced in physiological or pathological situations in vivo. We present evidence for one regulatory mechanism of human monocyte trafficking. Monocytes can integrate stimuli provided by inflammatory chemokines in the presence of homeostatic chemokines. In particular, migration and cell responses could occur at much lower concentrations of the CCR2 agonists, in the presence of chemokines (CCL19 and CCL21) that per se do not act on monocytes. Binding studies on CCR2 1 cells showed that CCL19 and CCL21 do not compete with the CCR2 agonist CCL2. Furthermore, the presence of CCL19 or CCL21 could influence the degradation of CCL2 and CCL7 on cells expressing the decoy receptor D6. These findings disclose a new scenario to further comprehend the complexity of chemokinebased monocyte trafficking in a vast variety of human inflammatory disorders.Key words: Chemokine receptors . Chemokines . Monocytes . Synergism IntroductionConcomitant exposure to multiple chemokines, the key controllers of several immune cell functions [1], can result in enhancement of immune responses. Only recently, a broad phenomenon known as ''chemokine synergism'' has been identified [2][3][4][5][6][7][8][9][10]. Cells expressing two or more chemokine receptors, in the presence of the selective agonists, can amplify their response [2][3][4][5][6]11]. The responses mediated by low agonist concentrations can be powerfully enhanced by non-ligand chemokines in cells that do not bear the second chemokine receptor [7][8][9]. Using different biochemical approaches, these studies demonstrated that CC and CXC chemokines form heteromeric complexes, which could endow the agonist with higher activity [7,9,12].Chemokines mediate their effects through interactions with heterotrimeric G-protein-coupled receptors [13][14][15]. Most leukocytes express more than one chemokine receptor and, hence, can respond to more than one chemokine. Additionally, a great variety of in situ experiments demonstrated the concomitant expression of chemokines at target sites of leukocyte trafficking and homing [16][17][18][19][20][21].Many chemokines, apart from being agonistic for their receptors, were shown to act as natural antagonists on one or several receptors in vitro and in vivo [22]. Naturally occurring N-terminal truncations of chemokines have been identified in vivo [23] and numerous enzymes were shown to generate truncations of chemokines that render them less active or inactive [24,25]. Therefore, there are strong indications that a cell needs to 1118integrate more than one signal provided by its environment and that environmental factors other than agonists might influence their responses.Chemokine production can be either constitutive or triggere...

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“…As CXCL12 is a chemokine with constitutive expression in many tissues (9,20,21), it is unlikely that it is alone responsible for pDC migration into sites of viral infection. Accordingly, it has been shown that CXCR4-mediated migration of pDCs is enhanced by CXCR3 ligand (CXCR3L) priming (14). This suggests that CXCR3 on pDCs functions solely as an amplifier of CXCR4-mediated chemotaxis.…”

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confidence: 99%

“…CXCR3 may also be the receptor guiding pDCs into virus-infected tissue, as its three ligands CXCL9, CXCL10, and CXCL11 are induced by IFN and are released rapidly after virus exposure (15)(16)(17)(18). However, CXCR3 on pDCs apparently does not mediate chemotaxis in vitro (12,14,19). This does not reflect an indigenous inability of pDCs to chemotax because CXCL12 can induce migration of these cells.…”

mentioning

confidence: 99%

“…Epitheliotropic DC precursors respond to the CCR6 ligand CCL20 (9,10), precursors of the dermal/interstitial-type DC lineage respond to CCR1/CCR5 and CCR2 ligands (9 -11), and pDC precursors/immature pDCs express CXCR4 and high levels of CXCR3, a receptor also present on Th1 and CTLs (6,(12)(13)(14). Accordingly, it has been speculated that L-selectin ϩ pDCs use CXCR3 to access T cell-rich areas of inflamed lymph nodes (6).…”

mentioning

confidence: 99%

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Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

Kohrgruber

Gröger

Meraner

et al. 2004

The Journal of Immunology

107

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Plasmacytoid dendritic cells (pDCs) recognize microbes, viruses in particular, and provide unique means of innate defense against them. The mechanism of pDC tissue recruitment remained enigmatic because the ligands of CXCR3, the cardinal chemokine receptor on pDCs, have failed to induce in vitro chemotaxis of pDCs in the absence of additional chemokines. In this study, we demonstrate that CXCR3 is sufficient to induce pDC migration, however, by a migratory mechanism that amalgamates the features of haptotaxis and chemorepulsion. To mediate “haptorepulsion” of pDCs, CXCR3 requires the encounter of its cognate ligands immobilized, optimally by heparan sulfate, in a form of a negative gradient. This is the first report of the absolute requirement of chemokine immobilization and presentation for its in vitro promigratory activity. The paradigmatic example of pDC haptorepulsion described here may represent a new pathophysiologically relevant migratory mechanism potentially used by other cells in response to other chemokines.

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The Inducible CXCR3 Ligands Control Plasmacytoid Dendritic Cell Responsiveness to the Constitutive Chemokine Stromal Cell–derived Factor 1 (SDF-1)/CXCL12

Cited by 221 publications

References 30 publications

Trafficking properties of plasmacytoid dendritic cells in health and disease

Trafficking properties of plasmacytoid dendritic cells in health and disease

Synergy‐inducing chemokines enhance CCR2 ligand activities on monocytes

Plasmacytoid Dendritic Cell Recruitment by Immobilized CXCR3 Ligands

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