Interferon gamma induces in human neutrophils and macrophages expression of the mRNA for the high affinity receptor for monomeric IgG (FcγR-I or CD64)

Cassatella, Marco Antonio; Flynn, R M; Amezaga, Miguel Aste; Bazzoni, Flavia; Vicentini, Federica; Trinchieri, Giorgio

doi:10.1016/0006-291x(90)92131-i

Cited by 64 publications

(43 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1, Fc␥RI mRNA expression is induced in human mast cells exposed to IFN-␥. This expression is maximal at 4 h in a kinetic pattern similar to that observed in neutrophils and monocytes (39). However, it should be noted that the RT-PCR techniques employed do not distinguish among Fc␥RIa, Fc␥RIb1, and Fc␥RIc.…”

Section: Discussionmentioning

confidence: 54%

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Okayama

Kirshenbaum

Metcalfe

2000

The Journal of Immunology

173

152

View full text Add to dashboard Cite

Biologically relevant activation of human mast cells through Fc receptors is believed to occur primarily through the high-affinity IgE receptor FcεRI. However, the demonstration in animal models that allergic reactions do not necessarily require Ag-specific IgE, nor the presence of a functional IgE receptor, and the clinical occurrence of some allergic reactions in situations where Ag-specific IgE appears to be lacking, led us to examine the hypothesis that human mast cells might express the high-affinity IgG receptor FcγRI and in turn be activated through aggregation of this receptor. We thus first determined by RT-PCR that resting human mast cells exhibit minimal message for FcγRI. We next found that IFN-γ up-regulated the expression of FcγRI. This was confirmed by flow cytometry, where FcγRI expression on human mast cells was increased from ∼2 to 44% by IFN-γ exposure. FcεRI, FcγRII, and FcγRIII expression was not affected. Scatchard plots were consisted with these data where the average binding sites for monomeric IgG1 (Ka = 4–5 × 108 M−1) increased from ∼2,400 to 12,100–17,300 per cell. Aggregation of FcγRI on human mast cells, and only after IFN-γ exposure, led to significant degranulation as evidenced by histamine release (24.5 ± 4.4%): and up-regulation of mRNA expression for specific cytokines including TNF-α, GM-CSF, IL-3 and IL-13. These findings thus suggest another mechanism by which human mast cells may be recruited into the inflammatory processes associated with some immunologic and infectious diseases.

show abstract

Section: Discussionmentioning

confidence: 54%

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Okayama

Kirshenbaum

Metcalfe

2000

The Journal of Immunology

173

152

View full text Add to dashboard Cite

show abstract

“…PBMC were isolated under endotoxin-free conditions 49 from the whole blood of healthy donors and 22 patients bearing colon adenocarcinoma (see Supplementary Table S4 for clinical details). slanDCs, CD1c þ DCs, pDCs and CD14 þ monocytes were isolated either from buffy coats of healthy donors and/or from the blood of CCR patients using specific isolation kits from Miltenyi Biotec, according to the manufacturer's instructions.…”

Section: Discussionmentioning

confidence: 99%

slanDCs selectively accumulate in carcinoma-draining lymph nodes and marginate metastatic cells

et al. 2014

Self Cite

View full text Add to dashboard Cite

Dendritic cells (DCs) initiate adaptive immune responses to cancer cells by activating naive T lymphocytes. 6-sulfo LacNAc þ DCs (slanDCs) represent a distinct population of circulating and tissue proinflammatory DCs, whose role in cancer immune surveillance is unknown. Herein, by screening a large set of clinical samples, we demonstrate accumulation of slanDCs in metastatic tumour-draining lymph nodes (M-TDLN) from carcinoma patients. Remarkably, slanDCs are absent at the primary carcinoma site, while their selective nodal recruitment follows the arrival of cancer cells to M-TDLN. slanDCs surround metastatic carcinoma deposits in close proximity to dead cells and efficiently phagocytose tumour cells. In colon carcinoma patients, the contingent of circulating slanDCs remains intact and competent in terms of IL-12p70 and tumour necrosis factor alpha production, induction of T-cell proliferation and migratory capacity to a set of chemokines produced in M-TDLN. We conclude that activated slanDCs represent previously unrecognized players of nodal immune responses to cancer cells.

show abstract

“…Highly purified granulocytes (neutrophils >96.5%, eosinophils <3%) and Percoll-purified monocytes were isolated and prepared under endotoxin-free conditions from buffy coats of healthy donors as previously described [11,31]. In some experiments, monocytes were also isolated by negative selection (to >95% purity) using MACS J separation (Monocyte Isolation kit II, from Miltenyi Biotec, Bergisch Gladbach, Germany).…”

Section: Cell Purification and Culturementioning

confidence: 99%

“…The resulting supernatants were immediately frozen in liquid nitrogen and stored at -80 C, while the corresponding pellets were either extracted for total RNA or lysed for protein analysis as described below. All reagents used were of the highest available grade and were dissolved in pyrogen-free water for clinical use [31].…”

Section: Cell Purification and Culturementioning

confidence: 99%

Molecular mechanisms underlying the synergistic induction of CXCL10 by LPS and IFN‐γ in human neutrophils

et al. 2007

Self Cite

View full text Add to dashboard Cite

The CXCL10 chemokine is a critical chemoattractant for the recruitment of activated Th1 and NK cells into inflammatory sites. CXCL10 is typically produced by myeloid cells in response to IFN-c, as well as by neutrophils, though the latter require a costimulation with IFN-c and LPS. In this study, we investigated the molecular mechanism(s) whereby IFN-c and TLR4 ligation synergize to induce CXCL10 expression in neutrophils. By primary transcript real-time PCR analysis, we demonstrate that the CXCL10 gene is transcriptionally induced by the LPS plus IFN-c combination in neutrophils, consistent with previous studies showing that increased CXCL10 gene expression does not reflect enhanced mRNA stability. The IFN-c-induced STAT1 activation and the lipopolysaccharide (LPS)-induced NF-jB activation were not enhanced if neutrophils were exposed to both stimuli, whereas both transcription factors were activated by IFN-c or LPS in monocytes. Finally, pharmacological inhibitors of NF-jB demonstrated its role in the induction of CXCL10 expression by LPS plus IFN-c in neutrophils, and by LPS or IFN-c in monocytes. Together, these results suggest that in neutrophils, the synergy observed between LPS and IFN-c toward CXCL10 gene expression likely reflects the cooperative induction of the NF-jB and STAT1 transcription factors by LPS and IFN-c, respectively. IntroductionCXCL10/IFN-c-inducible protein 10 (IP-10) is a critical component of several immune responses, acting notably as a chemoattractant for activated NK and Th1 cells into sites of inflammation. CXCL10 mediates its various activities by binding to CXCR3 expressed on activated Th1 and NK cells [1], and influences the behavior of nonimmune cells that express a CXCR3. For instance, it inhibits endothelial cell proliferation through interfering with the function of receptors for the growth factors, basic fibroblast growth factor and vascular endothelial growth factor, resulting in the inhibition of angiogenesis [2].Neutrophils are cells of the innate immune system that play an essential role in antimicrobial defense via the release of numerous toxic mediators [3]. In addition, extensive research has now clearly established that the release of chemokines and cytokines constitutes yet another key contribution of neutrophils to innate immunity (reviewed in reference [4]). Among the chemokines produced by neutrophils both in vitro and in vivo, CXCL10 stands out as being somewhat peculiar in terms of its induction characteristics, as originally shown by us [5,6] as well as by other groups [7][8][9]. Indeed, CXCL10 expression occurs in vitro only if However, the molecular bases of the particular inducibility of CXCL10 in human neutrophils have only been partially elucidated thus far. In this regard, we have recently clarified that the reason explaining the inability of LPS to induce CXCL10 mRNA expression in neutrophils reflects the fact that in this cell type, LPS is unable to mobilize the intracellular MyD88-independent pathway upon TLR4 binding [11]. As a result, LPS fails to...

show abstract

Interferon gamma induces in human neutrophils and macrophages expression of the mRNA for the high affinity receptor for monomeric IgG (FcγR-I or CD64)

Cited by 64 publications

References 19 publications

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

Expression of a Functional High-Affinity IgG Receptor, FcγRI, on Human Mast Cells: Up-Regulation by IFN-γ

slanDCs selectively accumulate in carcinoma-draining lymph nodes and marginate metastatic cells

Molecular mechanisms underlying the synergistic induction of CXCL10 by LPS and IFN‐γ in human neutrophils

Contact Info

Product

Resources

About