Reprint of Neutrophil cell surface receptors and their intracellular signal transduction pathways

Futosi, Krisztina; Fodor, Szabina; Mócsai, Attila

doi:10.1016/j.intimp.2013.11.010

Cited by 165 publications

(167 citation statements)

References 242 publications

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“…This suggests that Abl proteins play a key role in these FcγR functions. The Src kinase inhibitor PP2 also reduced ROS generation ( Figure 2A) and neutrophil adhesion to ICs under static conditions ( Figure 2C) as expected (18). The aforementioned studies evaluating the capture of human neutrophils on immobilized ICs were largely dependent on FcγRIIIB (10,11), which is GPI-linked but still signals via nonreceptor tyrosine kinase (29).…”

Section: Introductionsupporting

confidence: 71%

“…Next, the ability of library compounds to inhibit FcγRIIA + /γ -/--induced ROS was evaluated. Vehicle control (DMSO) and PP2, an inhibitor of Src family tyrosine kinases known to signal downstream of FcγRs (17,18), served as negative and positive controls, respectively. The screen of 8,483 compounds yielded 84 hits (1% hit rate), defined as those that have an inhibitory potential of ≥95% of PP2 ( Figure 1A).…”

Section: Resultsmentioning

confidence: 99%

“…FcγRIIA activation is initiated by ITAM phosphorylation, which triggers the docking of Syk and its phosphorylation by Src kinases that is followed by several downstream signals, including the phosphorylation and subsequent activation of the Rho GTPase guanine exchange factor Vav; Pyk-2 downstream of Syk; PI3K/Akt; MAPK/ ERK; and NADPH oxidase components such as p40 phox (17,18). Bosutinib inhibited FcγRIIA cross-linking-induced phosphorylation of these components as well as Crkl, a known Abl substrate (31) in FcγRIIA/γ -/-neutrophils (Supplemental Figure 3A).…”

Section: Resultsmentioning

confidence: 99%

See 2 more Smart Citations

Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases

Nishi

Furuhashi

Culleré

et al. 2017

Journal of Clinical Investigation

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Section: Introductionsupporting

confidence: 71%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases

Nishi

Furuhashi

Culleré

et al. 2017

Journal of Clinical Investigation

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“…Нейтрофильные грануло-циты выделяют ряд медиаторов -IL-8 (CXCL8), Gro-α (CXCL1), фактор комплемента С5а, кото-рые дополнительно рекрутируют и активируют новые нейтрофилы, создавая петлю обратной связи [39,43]. Кроме того, нейтрофильные гра-нулоциты секретируют интегрин Мас-1, моле-кулы адгезии L-селектин (CD62L) и PECAM-1 (CD31), которые являются ключевыми фактора-ми для миграции лейкоцитов к очагу воспаления, Toll-подобные рецепторы -TLR1, TLR2, TLR4 и TLR9, распознающие патоген-ассоциирован-ные молекулярные структуры [15,39]. Учитывая огромный арсенал секретируемых ферментов, цитокинов, хемокинов и рецепторов лигандов, нейтрофилы играют важную роль в инициации и поддержании хронического воспаления, в том числе при псориазе.…”

Section: участие цитокинов семейства Il-36 в патогене-зе псориатическunclassified

The Role of Cytokines of Interleukin 36 Family in Immunopathogenesis of Psoriasis

Пашкин¹,

Воробьева²,

Хайрутдинов³

et al. 2018

Med. immunol.

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“…Neutrophils serve crucial roles in the anti-bacterial and anti-fungal innate immune response and produce cytokines to initiate inflammatory responses; however, their inappropriate or excessive activation contributes to tissue damage during autoimmune and inflammatory diseases (1). Furthermore, the activity of neutrophils is associated with tumor progression, as demonstrated in colitis-associated cancer and glioblastoma (2,3).…”

Section: Introductionmentioning

confidence: 99%

MLN4924 suppresses lipopolysaccharide‑induced proinflammatory cytokine production in neutrophils in a dose‑dependent manner

Jin

Jing²,

Ye³

et al. 2018

Oncol Lett

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Abstract. Neddylation is a ubiquitination-like pathway. It has been reported that neddylation inhibition with the pharmacological agent MLN4924 potently uppresses lipopolysaccharide (LPS)-induced proinflammatory cytokine production, including tumor necrosis factor (TNF)-α and interleukin (IL)-6, by preventing the degradation of phosphorylated inhibitor of κB (p-IκB) in macrophages. However, whether neddylation serves a similar role in neutrophils remains unknown. In the present study MLN4924 treatment led to the accumulation of P-IκBα in neutrophils as well as the decreased production of TNF-α, IL-6 and IL-1β in response to LPS, in a dose-dependent manner. The viability of neutrophils was only marginally affected in the same conditions, without statistical significance. Furthermore, the nuclear factor (NF)-κB inhibitor JSH-23 mimicked the effects of MLN4924 in neutrophils, and the inhibitory effects of MLN4924 on LPS-induced proinflammatory cytokine production diminished in the presence of JSH-23. Thus, the results of the present study suggest that neddylation inhibition suppresses neutrophil function by suppressing the NF-κB signaling pathway. IntroductionNeutrophils serve crucial roles in the anti-bacterial and anti-fungal innate immune response and produce cytokines to initiate inflammatory responses; however, their inappropriate or excessive activation contributes to tissue damage during autoimmune and inflammatory diseases (1). Furthermore, the activity of neutrophils is associated with tumor progression, as demonstrated in colitis-associated cancer and glioblastoma (2,3).Previous studies have revealed that in order to protect the human body from invading pathogens and endogenous damage-associated molecules, neutrophils sense these threats through innate immune receptors, such as toll-like receptors (TLRs) and other pattern recognition receptors, to upregulate the secretion of inflammatory cytokines (4,5). The recognition of lipopolysaccharide (LPS) from gram-negative bacteria by TLR4 is a well-characterized example with the initiation of proinflammatory gene transcription through multiple signaling pathways, including nuclear factor (NF)-κB) (6,7). The exposure of neutrophils to bacterial LPS may contribute to tissue damage, under certain conditions, including endotoxic shock and infection-induced adult respiratory distress syndrome (8).Neddylation is a novel-type protein post-translational modification, a multistep enzymatic process that adds the ubiquitin-like molecule neural precursor cell expressed developmentally downregulated protein 8 (Nedd8) to target proteins in an ATP-dependent manner. Neddylation is vital for a range of processes, including cell viability, growth and development (9-12). To the best of our knowledge, the only known E1 for neddylation is a heterodimer comprised of the amyloid precursor protein-binding protein and ubiquitin-like modifier activating enzyme 3 (9-12). A previous study identified the ubiquitin-conjugating enzymes Ube2M and Ube2F as Nedd8 E2s (13). Several targets for N...

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Reprint of Neutrophil cell surface receptors and their intracellular signal transduction pathways

Cited by 165 publications

References 242 publications

Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases

Neutrophil FcγRIIA promotes IgG-mediated glomerular neutrophil capture via Abl/Src kinases

The Role of Cytokines of Interleukin 36 Family in Immunopathogenesis of Psoriasis

MLN4924 suppresses lipopolysaccharide‑induced proinflammatory cytokine production in neutrophils in a dose‑dependent manner

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