@article{MTMT:34786398,
	title = {Neutrophil IL-26 fuels autoinflammation},
	url = {https://m2.mtmt.hu/api/publication/34786398},
	author = {Futosi, Krisztina and Mócsai, Attila},
	doi = {10.1084/jem.20240229},
	journal-iso = {J EXP MED},
	journal = {JOURNAL OF EXPERIMENTAL MEDICINE},
	volume = {221},
	unique-id = {34786398},
	issn = {0022-1007},
	abstract = {Pustular psoriasis is an inflammatory skin disease with features of neutrophil-mediated sterile autoinflammation. In this issue of JEM, Baldo et al. show that this autoinflammation is driven by a vicious cycle through neutrophil-derived IL-26. Pustular psoriasis is an inflammatory skin disease with features of neutrophil-mediated sterile autoinflammation. In this issue of JEM, Baldo et al. (https://doi.org/10.1084/jem.20231464) show that this autoinflammation is driven by a vicious cycle through neutrophil-derived IL-26.},
	keywords = {immunology},
	year = {2024},
	eissn = {1540-9538},
	orcid-numbers = {Futosi, Krisztina/0000-0002-1661-4635; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:34728797,
	title = {Neutrophils and NADPH Oxidases Are Major Contributors to Mild but Not Severe Ischemic Acute Kidney Injury in Mice},
	url = {https://m2.mtmt.hu/api/publication/34728797},
	author = {Révész, Csaba and Kaucsár, Tamás and Godó, Mária and Bocskai, Krisztián and Krenács, Tibor and Mócsai, Attila and Szénási, Gábor and Hamar, Péter},
	doi = {10.3390/ijms25052948},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34728797},
	issn = {1661-6596},
	abstract = {Upregulation of free radical-generating NADPH oxidases (NOX), xanthine oxidoreductase (XOR), and neutrophil infiltration-induced, NOX2-mediated respiratory burst contribute to renal ischemia–reperfusion injury (IRI), but their roles may depend on the severity of IRI. We investigated the role of NOX, XOR, and neutrophils in developing IRI of various severities. C57BL/6 and Mcl-1ΔMyelo neutrophil-deficient mice were used. Oxidases were silenced by RNA interference (RNAi) or pharmacologically inhibited. Kidney function, morphology, immunohistochemistry and mRNA expression were assessed. After reperfusion, the expression of NOX enzymes and XOR increased until 6 h and from 15 h, respectively, while neutrophil infiltration was prominent from 3 h. NOX4 and XOR silencing or pharmacological XOR inhibition did not protect the kidney from IRI. Attenuation of NOX enzyme-induced oxidative stress by apocynin and neutrophil deficiency improved kidney function and ameliorated morphological damage after mild but not moderate/severe IRI. The IR-induced postischemic renal functional impairment (BUN, Lcn-2), tubular necrosis score, inflammation (TNF-α, F4/80), and decreases in the antioxidant enzyme (GPx3) mRNA expression were attenuated by both apocynin and neutrophil deficiency. Inhibition of NOX enzyme-induced oxidative stress or the lack of infiltration by NOX2-expressing neutrophils can attenuate reperfusion injury after mild but not moderate/severe renal IR.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Révész, Csaba/0000-0001-6016-526X; Kaucsár, Tamás/0000-0003-4460-1265; Krenács, Tibor/0000-0001-9164-065X; Mócsai, Attila/0000-0002-0512-1157; Szénási, Gábor/0000-0002-7350-6091; Hamar, Péter/0000-0002-1095-3564}
}

@article{MTMT:34596805,
	title = {Are Artificial Intelligence-Assisted Three-Dimensional Histological Reconstructions Reliable for the Assessment of Trabecular Microarchitecture?},
	url = {https://m2.mtmt.hu/api/publication/34596805},
	author = {Báskay, János and Pénzes, Dorottya and Kontsek, Endre and Pesti, Adrián István and Kiss, András and Carvalho, Bruna Katherine Guimarães and Szócska, Miklós and Szabó, Bence Tamás and Dobó-Nagy, Csaba and Csete, Dániel and Mócsai, Attila and Németh, Orsolya and Pollner, Péter and Mijiritsky, Eitan and Kivovics, Márton},
	doi = {10.3390/jcm13041106},
	journal-iso = {J CLIN MED},
	journal = {JOURNAL OF CLINICAL MEDICINE},
	volume = {13},
	unique-id = {34596805},
	abstract = {This study aimed to create a three-dimensional histological reconstruction through the AI-assisted classification of tissues and the alignment of serial sections. The secondary aim was to evaluate if the novel technique for histological reconstruction accurately replicated the trabecular microarchitecture of bone. This was performed by conducting micromorphometric measurements on the reconstruction and comparing the results obtained with those of microCT reconstructions. A bone biopsy sample was harvested upon re-entry following sinus floor augmentation. Following microCT scanning and histological processing, a modified version of the U-Net architecture was trained to categorize tissues on the sections. Detector-free local feature matching with transformers was used to create the histological reconstruction. The micromorphometric parameters were calculated using Bruker’s CTAn software (version 1.18.8.0, Bruker, Kontich, Belgium) for both histological and microCT datasets. Correlation coefficients calculated between the micromorphometric parameters measured on the microCT and histological reconstruction suggest a strong linear relationship between the two with ⍴-values of 0.777, 0.717, 0.705, 0.666, and 0.687 for BV/TV, BS/TV, Tb.Pf Tb.Th, and Tb.Sp, respectively. Bland–Altman and mountain plots suggest good agreement between BV/TV measurements on the two reconstruction methods. This novel method for three-dimensional histological reconstruction provides researchers with a tool that enables the assessment of accurate trabecular microarchitecture and histological information simultaneously.},
	year = {2024},
	eissn = {2077-0383},
	orcid-numbers = {Báskay, János/0000-0002-2841-3021; Kontsek, Endre/0000-0002-8098-1392; Pesti, Adrián István/0000-0001-6706-6221; Kiss, András/0000-0002-7453-3163; Szócska, Miklós/0000-0003-0648-9778; Szabó, Bence Tamás/0000-0002-5933-3956; Dobó-Nagy, Csaba/0000-0001-9530-7926; Csete, Dániel/0000-0001-8057-225X; Mócsai, Attila/0000-0002-0512-1157; Németh, Orsolya/0000-0002-4714-1463; Pollner, Péter/0000-0003-0464-4893; Mijiritsky, Eitan/0000-0002-1661-7529; Kivovics, Márton/0000-0003-0728-7027}
}

@article{MTMT:34543426,
	title = {The Syk inhibitor entospletinib abolishes dermal-epidermal separation in a fully human ex vivo model of bullous pemphigoid},
	url = {https://m2.mtmt.hu/api/publication/34543426},
	author = {Vikár, Simon and Szilveszter, Kata and Koszorú, Kamilla and Sárdy, Miklós and Mócsai, Attila},
	doi = {10.1016/j.jid.2024.01.009},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	unique-id = {34543426},
	issn = {0022-202X},
	year = {2024},
	eissn = {1523-1747},
	orcid-numbers = {Szilveszter, Kata/0000-0001-6185-7233; Sárdy, Miklós/0000-0003-4306-5093; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:34524564,
	title = {Surgical Treatment of Multiple Bone Cysts Using a Platelet-Rich Fibrin and BoneAlbumin Composite Graft: A Case Report},
	url = {https://m2.mtmt.hu/api/publication/34524564},
	author = {Major, Martin and Kivovics, Márton and Szabó, Bence Tamás and Déri, Tamás and Polyák, Melinda and Jákob, Noémi and Csete, Dániel and Mócsai, Attila and Németh, Zsolt and Szabó, György},
	doi = {10.3390/reports7010007},
	journal-iso = {REPORTS-BASEL},
	journal = {REPORTS},
	volume = {7},
	unique-id = {34524564},
	abstract = {Promising research results have been obtained on the tissue-regeneration properties of PRF (platelet-rich fibrin) in dentistry and maxillofacial surgery. PRF presumably promotes healing and accelerates ossification. In this case report, the patient had a history of Gorlin–Goltz syndrome, also called nevoid basal cell carcinoma syndrome, an autosomal dominant neurocutaneous disease that was known for many years. As a consequence, cysts were detected in both the mandible and maxilla. We performed decompression on this 37-year-old patient, followed by a cystectomy on an extensive lesion in the right angle of the mandible. One cyst from each side of the body mandible and one from the maxilla were completely enucleated, as determined using an intraoral exploration. The resulting bone defect was filled with a composite graft composed of a mixture of A-PRF and a serum albumin-coated bone allograft (BoneAlbumin). The wound was then covered with a PRF membrane. The surgical sites were closed per primam. The postoperative period was uneventful. Biopsies were performed after three and six months of healing for histological micromorphometry analyses. Dental implants were placed at the sampling site. Three months after the implantation, the ossified implants were fitted with superstructures. To date, no complications have appeared with the bone augmentation. The authors interpret from the findings that the combination of A-PRF and BoneAlbumin can be validated as a prosperous bone substitute. It can be safely implanted after a 3-month ossification period.},
	year = {2024},
	eissn = {2571-841X},
	orcid-numbers = {Kivovics, Márton/0000-0003-0728-7027; Szabó, Bence Tamás/0000-0002-5933-3956; Csete, Dániel/0000-0001-8057-225X; Mócsai, Attila/0000-0002-0512-1157; Németh, Zsolt/0000-0002-0231-7437; Szabó, György/0000-0002-5828-6078}
}

@article{MTMT:34424360,
	title = {The selective inhibition of the Syk tyrosine kinase ameliorates experimental autoimmune arthritis},
	url = {https://m2.mtmt.hu/api/publication/34424360},
	author = {Káposztás, Eszter Gertrúd and Balogh, Lili and Mócsai, Attila and Kemecsei, Éva and Jakus, Zoltán and Németh, Tamás},
	doi = {10.3389/fimmu.2023.1279155},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {14},
	unique-id = {34424360},
	issn = {1664-3224},
	abstract = {Autoimmune arthritis – such as rheumatoid arthritis – affect a significant proportion of the population, which can cause everyday joint pain, decreased mobility and reduced quality of life. Despite having more and more therapeutic options available, there are still a lot of patients who cannot reach remission or low disease activity by current therapies. This causes an urgent need for the development of new treatment options. The Syk tyrosine kinase plays an essential role in B cell receptor, Fc receptor and integrin signaling. It has been shown that the hematopoietic cell-specific deletion of Syk resulted in a complete protection against autoantibody-induced experimental arthritis. This prompted us to test the effect of entospletinib, a second generation, Syk-selective inhibitor, which has a tolerable safety profile according to hematological clinical trials, in experimental autoimmune arthritis. We found that entospletinib dose-dependently decreased the macroscopic signs of joint inflammation, while it did not affect the health status of the animals. In line with these findings, local neutrophil accumulation and cytokine levels were reduced compared to the vehicle-treated group, while macrophage accumulation and synovial fibroblast numbers were not significantly altered. Meanwhile, entospletinib dose-dependently decreased the cell responses of immune complex- or integrin ligand-activated neutrophils. Overall, we found that selective Syk inhibition by entospletinib reduced the activity of autoantibody-induced experimental arthritis, which seems to be based mainly on the effect of the inhibitor on neutrophil functions. Our data raise the possibility that entospletinib could be a good drug candidate in the treatment of human autoimmune arthritis.},
	year = {2023},
	eissn = {1664-3224},
	orcid-numbers = {Mócsai, Attila/0000-0002-0512-1157; Kemecsei, Éva/0000-0002-3602-7112; Jakus, Zoltán/0000-0002-6304-2369; Németh, Tamás/0000-0001-6854-4301}
}

@article{MTMT:34144235,
	title = {The authors reply},
	url = {https://m2.mtmt.hu/api/publication/34144235},
	author = {Florez-Barros, F. and Bearder, S. and Kull, B. and Freeman, A. and Mócsai, Attila and Robson, M.G.},
	doi = {10.1016/j.kint.2023.07.009},
	journal-iso = {KIDNEY INT},
	journal = {KIDNEY INTERNATIONAL},
	volume = {104},
	unique-id = {34144235},
	issn = {0085-2538},
	year = {2023},
	eissn = {1523-1755},
	pages = {856-857},
	orcid-numbers = {Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:33780028,
	title = {Lacking ARHGAP25 Mitigates the Symptoms of Autoantibodyinduced Arthritis in Mice},
	url = {https://m2.mtmt.hu/api/publication/33780028},
	author = {Czárán, Domonkos Tamás and Sasvári, Péter and Horváth, Ádám István and Ella, Krisztina and Südy, Ágnes and Borbély, Éva and Rusznák, Kitti and Czéh, Boldizsár and Mócsai, Attila and Helyes, Zsuzsanna and Csépányi-Kömi, Roland},
	doi = {10.3389/fimmu.2023.1182278},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {14},
	unique-id = {33780028},
	issn = {1664-3224},
	abstract = {Despite intensive research on rheumatoid arthritis, the pathomechanism of the disease is still not fully understood and the treatment has not been completely resolved. Previously we demonstrated that the GTPase-activating protein, ARHGAP25 has a crucial role in the regulation of basic phagocyte functions. Here we investigate the role of ARHGAP25 in the complex inflammatory process of autoantibody-induced arthritis.Wild-type and ARHGAP25 deficient (KO) mice on a C57BL/6 background, as well as bone marrow chimeric mice, were treated i.p. with the K/BxN arthritogenic or control serum, and the severity of inflammation and pain-related behavior was measured. Histology was prepared, leukocyte infiltration, cytokine production, myeloperoxidase activity, and superoxide production were determined, and comprehensive western blot analysis was conducted.In the absence of ARHGAP25, the severity of inflammation, joint destruction, and mechanical hyperalgesia significantly decreased, similarly to phagocyte infiltration, IL-1β, and MIP-2 levels in the tibiotarsal joint, whereas superoxide production or myeloperoxidase activity was unchanged. We observed a significantly mitigated phenotype in KO bone marrow chimeras as well. In addition, fibroblast-like synoviocytes showed comparable expression of ARHGAP25 to neutrophils. Significantly reduced ERK1/2, MAPK, and I-κB protein signals were detected in the arthritic KO mouse ankles.Our findings suggest that ARHGAP25 has a key role in the pathomechanism of autoantibody-induced arthritis in which it regulates inflammation via the I-κB/NF-κB/IL-1β axis with the involvement of both immune cells and fibroblast-like synoviocytes.},
	year = {2023},
	eissn = {1664-3224},
	orcid-numbers = {Ella, Krisztina/0000-0003-4961-5615; Südy, Ágnes/0000-0002-6759-4005; Borbély, Éva/0000-0002-1234-4391; Mócsai, Attila/0000-0002-0512-1157; Csépányi-Kömi, Roland/0000-0001-6825-7142}
}

@article{MTMT:33777508,
	title = {Analysis of intracellular tyrosine phosphorylation in circulating neutrophils as a rapid assay for the in vivo effect of oral tyrosine kinase inhibitors},
	url = {https://m2.mtmt.hu/api/publication/33777508},
	author = {Futosi, Krisztina and Bajza, Boglárka and Deli, Dorottya and Erdélyi, András and Tusnády, Simon and Mócsai, Attila},
	doi = {10.3389/fphar.2023.1056154},
	journal-iso = {FRONT PHARMACOL},
	journal = {FRONTIERS IN PHARMACOLOGY},
	volume = {14},
	unique-id = {33777508},
	abstract = {Tyrosine kinases are crucial signaling components of diverse biological processes and are major therapeutic targets in various malignancies and immune-mediated disorders. A critical step of development of novel tyrosine kinase inhibitors is the transition from the confirmation of the in vitro effects of drug candidates to the analysis of their in vivo efficacy. To facilitate this transition, we have developed a rapid in vivo assay for the analysis of the effect of oral tyrosine kinase inhibitors on basal tyrosine phosphorylation of circulating mouse neutrophils. The assay uses a single drop of peripheral blood without sacrificing the mice. Flow cytometry using intracellular staining by fluorescently labeled anti-phosphotyrosine antibodies revealed robust basal tyrosine phosphorylation in resting circulating neutrophils. This signal was abrogated by the use of isotype control antibodies or by pre-saturation of the anti-phosphotyrosine antibodies with soluble phosphotyrosine amino acids or tyrosine-phosphorylated peptides. Basal tyrosine phosphorylation was dramatically reduced in neutrophils of triple knockout mice lacking the Src-family tyrosine kinases Hck, Fgr, and Lyn. Neutrophil tyrosine phosphorylation was also abrogated by oral administration of the Abl/Src-family inhibitor dasatinib, a clinically used anti-leukemic agent. Detailed dose-response and kinetic studies revealed half-maximal reduction of neutrophil tyrosine phosphorylation by 2.9 mg/kg dasatinib, with maximal reduction observed 2 h after inhibitor administration. Taken together, our assay allows highly efficient analysis of the in vivo effect of orally administered tyrosine kinase inhibitors, and may be used as a suitable alternative to other existing approaches.},
	year = {2023},
	eissn = {1663-9812},
	orcid-numbers = {Futosi, Krisztina/0000-0002-1661-4635; Bajza, Boglárka/0000-0003-1203-3603; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:33770181,
	title = {Myeloid Src-family kinases are critical for neutrophil-mediated autoinflammation in gout and motheaten models.},
	url = {https://m2.mtmt.hu/api/publication/33770181},
	author = {Futosi, Krisztina and Németh, Tamás and Horváth, Ádám István and Abram, Clare L and Tusnády, Simon and Lowell, Clifford A and Helyes, Zsuzsanna and Mócsai, Attila},
	doi = {10.1084/jem.20221010},
	journal-iso = {J EXP MED},
	journal = {JOURNAL OF EXPERIMENTAL MEDICINE},
	volume = {220},
	unique-id = {33770181},
	issn = {0022-1007},
	abstract = {Autoinflammatory diseases include a number of monogenic systemic inflammatory diseases, as well as acquired autoinflammatory diseases such as gout. Here, we show that the myeloid Src-family kinases Hck, Fgr, and Lyn are critical for experimental models of gout, as well as for genetically determined systemic inflammation in the Ptpn6me-v/me-v (motheaten viable) mouse model. The Hck-/-Fgr-/-Lyn-/- mutation abrogated various monosodium urate (MSU) crystal-induced pro-inflammatory responses of neutrophils, and protected mice from the development of gouty arthritis. The Src-family inhibitor dasatinib abrogated MSU crystal-induced responses of human neutrophils and reduced experimental gouty arthritis in mice. The Hck-/-Fgr-/-Lyn-/- mutation also abrogated spontaneous inflammation and prolonged the survival of the Ptpn6me-v/me-v mice. Spontaneous adhesion and superoxide release of Ptpn6me-v/me-v neutrophils were also abolished by the Hck-/-Fgr-/-Lyn-/- mutation. Excessive activation of tyrosine phosphorylation pathways in myeloid cells may characterize a subset of autoinflammatory diseases.},
	year = {2023},
	eissn = {1540-9538},
	orcid-numbers = {Futosi, Krisztina/0000-0002-1661-4635; Németh, Tamás/0000-0001-6854-4301; Mócsai, Attila/0000-0002-0512-1157}
}