@article{MTMT:1844642,
	title = {Angiotensin II type 1-receptor activating antibodies in renal-allograft rejection},
	url = {https://m2.mtmt.hu/api/publication/1844642},
	author = {Dragun, D and Muller, DN and Brasen, JH and Fritsche, L and Nieminen-Kelha, M and Dechend, R and Kintscher, U and Rudolph, B and Hoebeke, J and Eckert, D and Mazák, István and Plehm, R and Schonemann, C and Unger, T and Budde, K and Neumayer, HH and Luft, FC and Wallukat, G},
	doi = {10.1056/NEJMoa035717},
	journal-iso = {NEW ENGL J MED},
	journal = {NEW ENGLAND JOURNAL OF MEDICINE},
	volume = {352},
	unique-id = {1844642},
	issn = {0028-4793},
	abstract = {BACKGROUND Antibodies against HLA antigens cause refractory allograft rejection with vasculopathy in some, but not all, patients. METHODS We studied 33 kidney-transplant recipients who had refractory vascular rejection. Thirteen had donor-specific anti-HLA antibodies, whereas 20 did not. Malignant hypertension was present in 16 of the patients without anti- HLA antibodies, 4 of whom had seizures. The remaining 17 patients had no malignant hypertension. We hypothesized that activating antibodies targeting the angiotensin II type 1 (AT(1)) receptor might be involved. RESULTS Activating IgG antibodies targeting the AT(1) receptor were detected in serum from all 16 patients with malignant hypertension and without anti- HLA antibodies, but in no other patients. These receptor-activating antibodies are subclass IgG1 and IgG3 antibodies that bind to two different epitopes on the second extracellular loop of the AT(1) receptor. Tissue factor expression was increased in renal-biopsy specimens from patients with these antibodies. In vitro stimulation of vascular cells with an AT(1)-receptor-activating antibody induced phosphorylation of ERK 1/2 kinase and increased the DNA binding activity of the transcription factors activator protein 1 (AP-1) and nuclear factor-kappaB. The AT(1) antagonist losartan blocked agonistic AT(1) - receptor antibody - mediated effects, and passive antibody transfer induced vasculopathy and hypertension in a rat kidney-transplantation model. CONCLUSIONS A non-HLA, AT(1) - receptor - mediated pathway may contribute to refractory vascular rejection, and affected patients might benefit from removal of AT(1) - receptor antibodies or from pharmacologic blockade of AT(1) receptors.},
	keywords = {ENDOTHELIAL-CELLS; INJURY; CLASSIFICATION; TRANSPLANTATION; DILATED CARDIOMYOPATHY; AT(1) receptor; TISSUE FACTOR; C4D DEPOSITION; VASCULAR REJECTION; AGONISTIC ANTIBODIES},
	year = {2005},
	eissn = {1533-4406},
	pages = {558-569}
}

@article{MTMT:31285571,
	title = {Non-HLA transplantation immunity revealed by lymphocytotoxic antibodies},
	url = {https://m2.mtmt.hu/api/publication/31285571},
	author = {Opelz, Gerhard},
	doi = {10.1016/s0140-6736(05)66458-6},
	journal-iso = {LANCET},
	journal = {LANCET},
	volume = {365},
	unique-id = {31285571},
	issn = {0140-6736},
	keywords = {Histocompatibility Testing; Living Donors},
	year = {2005},
	eissn = {1474-547X},
	pages = {1570-1576},
	orcid-numbers = {Szederkényi, Edit/0000-0002-3583-6874}
}

@article{MTMT:1029117,
	title = {Childhood membranous nephropathy, circulating antibodies to the 58-kD TIN antigen, and anti-tubular basement membrane nephritis: An 11-year follow-up},
	url = {https://m2.mtmt.hu/api/publication/1029117},
	author = {Iványi, Béla and Haszon, I and Börcsökné Endreffy, Emőke and Szenohradszky, Pál and Petri, I B and Kalmár, Tibor and Butkowski, R J and Charonis, A S and Túri, Sándor},
	doi = {10.1016/S0272-6386(98)70085-X},
	journal-iso = {AM J KIDNEY DIS},
	journal = {AMERICAN JOURNAL OF KIDNEY DISEASES},
	volume = {32},
	unique-id = {1029117},
	issn = {0272-6386},
	year = {1998},
	eissn = {1523-6838},
	pages = {1068-1074},
	orcid-numbers = {Börcsökné Endreffy, Emőke/0000-0002-2695-6495; Kalmár, Tibor/0000-0002-0419-2009}
}