Signal Relay by CC Chemokine Receptor 2 (CCR2) and Formylpeptide Receptor 2 (Fpr2) in the Recruitment of Monocyte-derived Dendritic Cells in Allergic Airway Inflammation

Chen, Keqiang; Liu, Mingyong; Liu, Ying; Wang, Chunyan; Yoshimura, Teizo; Gong, Wanghua; Le, Yingying; Tessarollo, Lino; Wang, Ji Ming

doi:10.1074/jbc.m113.450635

Cited by 42 publications

(44 citation statements)

References 51 publications

(61 reference statements)

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“…CCR2 is a chemokine receptor expressed on the cell surface of inflammatory monocytes and moDCs and is involved with facilitating their migration to sites of inflammation (24,25). Indeed, the absence of CCR2 has been found to result in a significant reduction in the recruitment of moDCs in response to infection (26,27) or allergic disease (28). Consistent with previous reports of moDCs arising in other inflammatory contexts, we confirmed that the allogeneic Ag-induced splenic moDCs we observed were CCR2 + (Fig.…”

supporting

confidence: 81%

Innate Allorecognition Results in Rapid Accumulation of Monocyte-Derived Dendritic Cells

Chow

Delconte

Huntington

et al. 2016

The Journal of Immunology

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Although the mechanisms governing the innate recognition of pathogen-associated molecular patterns have been well defined, how allogeneic cellular stimuli evoke innate responses remains less so. In this article, we report that upon i.v. transfer (to avoid major iatrogenic interference), allogeneic but not syngeneic leukocytes could induce a rapid (after 1 d) accumulation of host monocyte–derived dendritic cells (moDCs) without any increase in conventional DCs. This occurred in various donor–host strain combinations, did not require MHC mismatch, and could be induced by various donor cell types including B cells, T cells, or NK cells. Using RAG−/−γc−/− and scid γc−/−mice with different MHC, we found that the presence of either donor or host lymphoid cells was required. Alloinduced moDC accumulation was significantly reduced when splenocytes from mice deficient in NK cells by genetic ablation were used as donors. A major component of this moDC accumulation appears to be recruitment. Our findings provide new insights into how the innate and adaptive immune system may interact during allogeneic encounters and thus transplant rejection.

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supporting

confidence: 81%

Innate Allorecognition Results in Rapid Accumulation of Monocyte-Derived Dendritic Cells

Chow

Delconte

Huntington

et al. 2016

The Journal of Immunology

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“…Whereas activation of FPRL1 by serum amyloid A induced CCL2 production in human endothelial cells, CCL2 acts synergistically with FPR ligand fMLF. 44,45 Chen et al 46 demonstrated that interaction of the chemokine receptor CCR2, the receptor for CCL2, and FPR2 with their endogenous ligands sequentially mediated the trafficking of dendritic cells within the inflamed lung. Our in vitro results with glial cell stimulation showed that the lack of FPR1 resulted in a comparable to stronger induction of chemokine expression compared with WT glia cells, whereas FPR2 deficiency led to attenuated over-expression.…”

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confidence: 99%

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

et al. 2014

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SummaryBacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause of severe neuronal sequelae. The brain is protected from penetrating pathogens by both the blood-brain barrier and the innate immune system. The invading pathogens are recognized by pattern recognition receptors including the G-protein coupled formyl peptide receptors (FPRs), which are expressed by immune cells of the central nervous system. The expression of FPRs is up-regulated during bacterial meningitis, but the consequence on the progression of inflammation and impact on mortality are far from clear. Therefore, we used mFPR1 and mFPR2-deficient mice to investigate the effects on inflammation, bacterial growth and mortality in a mouse model of pneumococcal meningitis. Our results revealed increased bacterial burden, increased neutrophil infiltration and higher mortality in mFPR1/2-deficient mice in comparison to wild-type mice. The mFPR1-or mFPR2-deficient mice also showed significantly increased glial cell density, whereas the immune responses including the expression of anti-inflammatory cytokines and antimicrobial peptides were decreased in bacterial meningitis. Taken together, the results suggest that FPR1 and FPR2 play an important role in the innate immune responses against Streptococcus pneumoniae within the central nervous system and the lack of the receptors leads to a dysregulation of the inflammatory response compared with wild-type mice.

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“…Further investigation revealed that there is a significantly reduced recruitment of Ly6C ϩ inflammatory DCs into the bronchiolar area in the allergic inflammatory airway of Fpr2 Ϫ/Ϫ or CRAMP Ϫ/Ϫ mice, suggesting that Fpr2 and its endogenous ligand CRAMP control DC trafficking (1).…”

mentioning

confidence: 99%

“…Leukocyte trafficking and homing are mediated by G protein-coupled receptors (GPCRs) 3 that recognize pathogen and host-derived chemoattractants (1,2). Some chemoattractant GPCRs are involved in both innate and adaptive immune responses (3) and are essential for development, angiogenesis, and homing of antigen presenting dendritic cells (DCs) (4).…”

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confidence: 99%

The Formylpeptide Receptor 2 (Fpr2) and Its Endogenous Ligand Cathelin-related Antimicrobial Peptide (CRAMP) Promote Dendritic Cell Maturation

Chen

Xiang

Huang

et al. 2014

Journal of Biological Chemistry

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Background: Chemoattractant receptor Fpr2 interacts with host-derived agonist CRAMP and promotes dentritic cell maturation in immune responses. Results: Deficiency in Fpr2 or CRAMP results in impaired maturation of dendritic cells in vitro and in vivo.Conclusion: Fpr2 and its agonist CRAMP play a nonredundant role in DC maturation. Significance: Fpr2 and its agonist CRAMP are potential targets for disease intervention.

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Signal Relay by CC Chemokine Receptor 2 (CCR2) and Formylpeptide Receptor 2 (Fpr2) in the Recruitment of Monocyte-derived Dendritic Cells in Allergic Airway Inflammation

Cited by 42 publications

References 51 publications

Innate Allorecognition Results in Rapid Accumulation of Monocyte-Derived Dendritic Cells

Innate Allorecognition Results in Rapid Accumulation of Monocyte-Derived Dendritic Cells

Lack of formyl peptide receptor 1 and 2 leads to more severe inflammation and higher mortality in mice with of pneumococcal meningitis

The Formylpeptide Receptor 2 (Fpr2) and Its Endogenous Ligand Cathelin-related Antimicrobial Peptide (CRAMP) Promote Dendritic Cell Maturation

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