On the cytokines produced by human neutrophils in tumors

Tecchio, Cristina; Scapini, Patrizia; Pizzolo, Giovanni; Cassatella, Marco A.

doi:10.1016/j.semcancer.2013.02.004

Cited by 160 publications

(140 citation statements)

References 149 publications

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“…58 Conversely, recent in vivo data confirm that splenic mouse neutrophils support preimmune immunoglobulin (Ig)G3 production, as well as postimmune IgM, IgG2b, IgG2c, and IgG3 responses to repetitive immunization with polysaccharides such as 2,4,6-trinitrophenyl-ficoll (A. Chorny and A. Cerutti, unpublished data, 2014). Neutrophils have also been proposed to play a role in the pathogenesis of B-cell lymphomas, either through the production of APRIL 59 or, based on studies in mice, through NET release 60 (supplemental Table 2). Neutrophils and T cells.…”

Section: Cross-talk Between Neutrophils and Adaptive Immune Cellsmentioning

confidence: 99%

“…59,107,108 Current evidence mostly support the idea that neutrophils facilitate, rather than inhibit, cancer progression primarily through their ability to promote tumor angiogenesis, invasion, and metastasis. [107][108][109][110] This concept is also supported by dozens of reports correlating elevated numbers of tumor-infiltrating and/or blood neutrophils, as well as elevated blood neutrophil/ lymphocyte ratios, with poor clinical outcome in several cancers.…”

Section: Neutrophils In Cancermentioning

confidence: 99%

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Social networking of human neutrophils within the immune system

Scapini

Cassatella

2014

Blood

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335

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It is now widely recognized that neutrophils are highly versatile and sophisticated cells that display de novo synthetic capacity and may greatly extend their lifespan. In addition, concepts such as “neutrophil heterogeneity” and “neutrophil plasticity” have started to emerge, implying that, under pathological conditions, neutrophils may differentiate into discrete subsets defined by distinct phenotypic and functional profiles. A number of studies have shown that neutrophils act as effectors in both innate and adaptive immunoregulatory networks. In fact, once recruited into inflamed tissues, neutrophils engage into complex bidirectional interactions with macrophages, natural killer, dendritic and mesenchymal stem cells, B and T lymphocytes, or platelets. As a result of this cross-talk, mediated either by contact-dependent mechanisms or cell-derived soluble factors, neutrophils and target cells reciprocally modulate their survival and activation status. Altogether, these novel aspects of neutrophil biology have shed new light not only on the potential complex roles that neutrophils play during inflammation and immune responses, but also in the pathogenesis of several inflammatory disorders including infection, autoimmunity, and cancer.

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Section: Cross-talk Between Neutrophils and Adaptive Immune Cellsmentioning

confidence: 99%

Section: Neutrophils In Cancermentioning

confidence: 99%

Social networking of human neutrophils within the immune system

Scapini

Cassatella

2014

Blood

Self Cite

335

305

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“…Although neutrophils release only small quantities of cytokines, neutrophil-derived mediators have been shown to play an important role in the pathogenesis of multiple conditions, including arthritis (39), cancer (40), and HIV infection (41). We measured cytokine release by neutrophils after 24 h of coculture with axenic amastigotes or metacyclic promastigotes.…”

Section: Leishmania Amastigotes Resist Killing By Neutrophilsmentioning

confidence: 99%

Leishmania amazonensis Amastigotes Trigger Neutrophil Activation but Resist Neutrophil Microbicidal Mechanisms

et al. 2013

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Neutrophils are the first cells to infiltrate to the site of Leishmania promastigote infection, and these cells help to reduce parasite burden shortly after infection is initiated. Several clinical reports indicate that neutrophil recruitment is sustained over the course of leishmaniasis, and amastigote-laden neutrophils have been isolated from chronically infected patients and experimentally infected animals. The goal of this study was to compare how thioglycolate-elicited murine neutrophils respond to L. amazonensis metacyclic promastigotes and amastigotes derived from axenic cultures or from the lesions of infected mice. Neutrophils efficiently internalized both amastigote and promastigote forms of the parasite, and phagocytosis was enhanced in lipopolysaccharide (LPS)-activated neutrophils or when parasites were opsonized in serum from infected mice. Parasite uptake resulted in neutrophil activation, oxidative burst, and accelerated neutrophil death. While promastigotes triggered the release of tumor necrosis factor alpha (TNF-␣), uptake of amastigotes preferentially resulted in the secretion of interleukin-10 (IL-10) from neutrophils. Finally, the majority of promastigotes were killed by neutrophils, while axenic culture-and lesion-derived amastigotes were highly resistant to neutrophil microbicidal mechanisms. This study indicates that neutrophils exhibit distinct responses to promastigote and amastigote infection. Our findings have important implications for determining the impact of sustained neutrophil recruitment and amastigote-neutrophil interactions during the late phase of cutaneous leishmaniasis.

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“…Neutrophils produce a proliferation inducing ligand (APRIL, TNFSF13) (13). The initial reported function of APRIL was induction of increased proliferation in tumor cells (14).…”

Section: Introductionmentioning

confidence: 99%

CXCL-8/IL8 Produced by Diffuse Large B-cell Lymphomas Recruits Neutrophils Expressing a Proliferation-Inducing Ligand APRIL

et al. 2017

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Tumor-infiltrating neutrophils have been implicated in malignant development and progression, but mechanisms are ill defined. Neutrophils produce a proliferation-inducing ligand APRIL/TNFSF13, a factor that promotes development of tumors from diverse origins, including diffuse large B-cell lymphoma (DLBCL). High APRIL expression in DLBCL correlates with reduced patient survival, but the pathway(s) dictating APRIL expression are not known. Here, we show that all blood neutrophils constitutively secrete APRIL, and inflammation-associated stimuli, such as TNF, further upregulate APRIL. In a significant fraction of DLBCL patients, tumor cells constitutively produced the ELC-CXC chemokine CXCL-8 (IL8), enabling them to recruit APRIL-producing blood neutrophils. CXCL-8 production in DLBCL was unrelated to the cell of origin, as APRIL-producing neutrophils infiltrated CXCL-8+ DLBCL from both germinal center (GC) and non-GC subtypes. Rather, CXCL-8 production implied events affecting DNA methylation and acetylation. Overall, our results showed that chemokine-mediated recruitment of neutrophils secreting the tumor-promoting factor APRIL mediates DLBCL progression. Cancer Res; 77(5); 1097–107. ©2016 AACR.

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On the cytokines produced by human neutrophils in tumors

Cited by 160 publications

References 149 publications

Social networking of human neutrophils within the immune system

Social networking of human neutrophils within the immune system

Leishmania amazonensis Amastigotes Trigger Neutrophil Activation but Resist Neutrophil Microbicidal Mechanisms

CXCL-8/IL8 Produced by Diffuse Large B-cell Lymphomas Recruits Neutrophils Expressing a Proliferation-Inducing Ligand APRIL

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