@article{MTMT:34775042,
	title = {Novel and potential future therapeutic options in systemic autoimmune diseases},
	url = {https://m2.mtmt.hu/api/publication/34775042},
	author = {Balogh, Lili and Olah, Katalin and Santa, Soma and Majerhoffer, Nora and Németh, Tamás},
	doi = {10.3389/fimmu.2024.1249500},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {15},
	unique-id = {34775042},
	issn = {1664-3224},
	abstract = {Autoimmune inflammation is caused by the loss of tolerance to specific self-antigens and can result in organ-specific or systemic disorders. Systemic autoimmune diseases affect a significant portion of the population with an increasing rate of incidence, which means that is essential to have effective therapies to control these chronic disorders. Unfortunately, several patients with systemic autoimmune diseases do not respond at all or just partially respond to available conventional synthetic disease-modifying antirheumatic drugs and targeted therapies. However, during the past few years, some new medications have been approved and can be used in real-life clinical settings. Meanwhile, several new candidates appeared and can offer promising novel treatment options in the future. Here, we summarize the newly available medications and the most encouraging drug candidates in the treatment of systemic lupus erythematosus, rheumatoid arthritis, Sjogren's disease, systemic sclerosis, systemic vasculitis, and autoimmune myositis.},
	keywords = {INHIBITOR; SAFETY; RHEUMATOID-ARTHRITIS; ANTIBODY; EFFICACY; placebo; autoimmune disease; DOUBLE-BLIND; treatment; PRIMARY SJOGRENS-SYNDROME; Pathomechanism; LUPUS-ERYTHEMATOSUS; PHASE-2 TRIAL; EOSINOPHILIC GRANULOMATOSIS},
	year = {2024},
	eissn = {1664-3224},
	orcid-numbers = {Németh, Tamás/0000-0001-6854-4301}
}

@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: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}
}

@article{MTMT:33623361,
	title = {Neutrophil-specific Syk expression is crucial for skin disease in experimental epidermolysis bullosa acquisita},
	url = {https://m2.mtmt.hu/api/publication/33623361},
	author = {Németh, Tamás and Balogh, Lili and Káposztás, Eszter Gertrúd and Szilveszter, Kata and Mócsai, Attila},
	doi = {10.1016/j.jid.2022.12.016},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	volume = {143},
	unique-id = {33623361},
	issn = {0022-202X},
	year = {2023},
	eissn = {1523-1747},
	pages = {1147-1156},
	orcid-numbers = {Németh, Tamás/0000-0001-6854-4301; Szilveszter, Kata/0000-0001-6185-7233; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:32923734,
	title = {Synovial fibroblasts as potential drug targets in rheumatoid arthritis, where do we stand and where shall we go?},
	url = {https://m2.mtmt.hu/api/publication/32923734},
	author = {Németh, Tamás and Nagy, György and Pap, Thomas},
	doi = {10.1136/annrheumdis-2021-222021},
	journal-iso = {ANN RHEUM DIS},
	journal = {ANNALS OF THE RHEUMATIC DISEASES},
	volume = {81},
	unique-id = {32923734},
	issn = {0003-4967},
	abstract = {Fibroblast-like synoviocytes or synovial fibroblasts (FLS) are important cellular components of the inner layer of the joint capsule, referred to as the synovial membrane. They can be found in both layers of this synovial membrane and contribute to normal joint function by producing extracellular matrix components and lubricants. However, under inflammatory conditions like in rheumatoid arthritis (RA), they may start to proliferate, undergo phenotypical changes and become central elements in the perpetuation of inflammation through their direct and indirect destructive functions. Their importance in autoimmune joint disorders makes them attractive cellular targets, and as mesenchymal-derived cells, their inhibition may be carried out without immunosuppressive consequences. Here, we aim to give an overview of our current understanding of the target potential of these cells in RA.},
	keywords = {TISSUE; EXPRESSION; INHIBITION; T-CELLS; ARTHRITIS; FIBROBLASTS; INVASION; HYPOXIA; cadherin-11; rheumatoid; Synoviocytes; INTRINSIC REGULATOR},
	year = {2022},
	eissn = {1468-2060},
	pages = {1055-1064},
	orcid-numbers = {Németh, Tamás/0000-0001-6854-4301; Nagy, György/0000-0003-1198-3228; Pap, Thomas/0000-0001-6514-0416}
}

@article{MTMT:32169581,
	title = {Signaling through Syk or CARD9 Mediates Species-Specific Anti-Candida Protection in Bone Marrow Chimeric Mice},
	url = {https://m2.mtmt.hu/api/publication/32169581},
	author = {Zajta, Erik and Csonka, Katalin and Tóth, Adél and Tiszlavicz, László and Németh, Tamás and Orosz, Anita and Novák, Ádám and Csikós, Máté Lajos and Vágvölgyi, Csaba and Mócsai, Attila and Gácser, Attila},
	doi = {10.1128/mBio.01608-21},
	journal-iso = {MBIO},
	journal = {MBIO},
	volume = {12},
	unique-id = {32169581},
	issn = {2161-2129},
	year = {2021},
	eissn = {2150-7511},
	orcid-numbers = {Zajta, Erik/0000-0001-5258-2506; Tiszlavicz, László/0000-0003-1134-6587; Németh, Tamás/0000-0001-6854-4301; Vágvölgyi, Csaba/0000-0003-0009-7773; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:31156872,
	title = {Neutrophils as emerging therapeutic targets},
	url = {https://m2.mtmt.hu/api/publication/31156872},
	author = {Németh, Tamás and Sperandio, M. and Mócsai, Attila},
	doi = {10.1038/s41573-019-0054-z},
	journal-iso = {NAT REV DRUG DISCOV},
	journal = {NATURE REVIEWS DRUG DISCOVERY},
	volume = {19},
	unique-id = {31156872},
	issn = {1474-1776},
	abstract = {Neutrophils are the most abundant circulating leukocytes, being the first line of defence against bacterial and fungal infections. However, neutrophils also contribute to tissue damage during various autoimmune and inflammatory diseases, and play important roles in cancer progression. The intimate but complex involvement of neutrophils in various diseases makes them exciting targets for therapeutic intervention but also necessitates differentiation of beneficial responses from potentially detrimental side effects. A variety of approaches to therapeutically target neutrophils have emerged, including strategies to enhance, inhibit or restore neutrophil function, with several agents entering clinical trials. However, challenges and controversies in the field remain. © 2020, Springer Nature Limited.},
	year = {2020},
	eissn = {1474-1784},
	pages = {253-275},
	orcid-numbers = {Németh, Tamás/0000-0001-6854-4301; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:31900984,
	title = {Neutrophil-specific deletion of the Syk tyrosine kinase abrogates the development of experimental epidermolysis bullosa acquisita},
	url = {https://m2.mtmt.hu/api/publication/31900984},
	author = {Németh, Tamás and Szilveszter, Kata and Sitaru, Cassian and Mócsai, Attila},
	journal-iso = {EUR J CLIN INVEST},
	journal = {EUROPEAN JOURNAL OF CLINICAL INVESTIGATION},
	volume = {49},
	unique-id = {31900984},
	issn = {0014-2972},
	year = {2019},
	eissn = {1365-2362},
	pages = {139-139},
	orcid-numbers = {Németh, Tamás/0000-0001-6854-4301; Szilveszter, Kata/0000-0001-6185-7233; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:31900972,
	title = {Investigating the role of PLC gamma 2 in autoimmune skin inflammation},
	url = {https://m2.mtmt.hu/api/publication/31900972},
	author = {Szilveszter, Kata and Németh, Tamás and Mócsai, Attila},
	doi = {10.1111/eci.13110},
	journal-iso = {EUR J CLIN INVEST},
	journal = {EUROPEAN JOURNAL OF CLINICAL INVESTIGATION},
	volume = {49},
	unique-id = {31900972},
	issn = {0014-2972},
	year = {2019},
	eissn = {1365-2362},
	pages = {135-135},
	orcid-numbers = {Szilveszter, Kata/0000-0001-6185-7233; Németh, Tamás/0000-0001-6854-4301; Mócsai, Attila/0000-0002-0512-1157}
}

@article{MTMT:31900946,
	title = {Characterizing the Role of PLC gamma 2 in Autoantibody-induced Skin Inflammation},
	url = {https://m2.mtmt.hu/api/publication/31900946},
	author = {Szilveszter, Kata and Németh, Tamás and Mócsai, Attila},
	doi = {10.1016/j.jid.2019.07.381},
	journal-iso = {J INVEST DERMATOL},
	journal = {JOURNAL OF INVESTIGATIVE DERMATOLOGY},
	volume = {139},
	unique-id = {31900946},
	issn = {0022-202X},
	year = {2019},
	eissn = {1523-1747},
	pages = {S279-S279},
	orcid-numbers = {Szilveszter, Kata/0000-0001-6185-7233; Németh, Tamás/0000-0001-6854-4301; Mócsai, Attila/0000-0002-0512-1157}
}