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001-es BibID:	BIBFORM096506
Első szerző:	Iversen, Rasmus
Cím:	Efficient T cell-B cell collaboration guides autoantibody epitope bias and onset of celiac disease / Iversen Rasmus, Roy Bishnudeo, Stamnaes Jorunn, Hydahl Lene S., Hnida Kathrin, Neumann Ralf S., Korponay-Szabó Ilma R., Lundin Knut E. A., Sollid Ludvig M.
Dátum:	2019
ISSN:	0027-8424 1091-6490
Megjegyzések:	B cells play important roles in autoimmune diseases through autoantibody production, cytokine secretion, or antigen presentation to T cells. In most cases, the contribution of B cells as antigenpresenting cells is not well understood. We have studied the autoantibody response against the enzyme transglutaminase 2 (TG2) in celiac disease patients by generating recombinant antibodies from single gut plasma cells reactive with discrete antigen domains and by undertaking proteomic analysis of anti-TG2 serum antibodies. The majority of the cells recognized epitopes in the Nterminal domain of TG2. Antibodies recognizing C-terminal epitopes interfered with TG2 cross-linking activity, and B cells specific for Cterminal epitopes were inefficient at taking up TG2-gluten complexes for presentation to gluten-specific T cells. The bias toward N-terminal epitopes hence reflects efficient T-B collaboration. Production of antibodies against N-terminal epitopes coincided with clinical onset of disease, suggesting that TG2-reactive B cells with certain epitope specificities could be the main antigen-presenting cells for pathogenic, gluten-specific T cells. The link between B cell epitopes, antigen presentation, and disease onset provides insight into the pathogenic mechanisms of a T cell-mediated autoimmune condition.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk celiac disease B cells antigen presentation autoantibodies celiac disease
Megjelenés:	Proceedings Of The National Academy Of Sciences Of The United States Of America. - 116 : 30 (2019), p. 15134-15139. -
További szerzők:	Roy, Bishnudeo Stamnaes, Jorunn Hydahl, Lene S. Hnida, Kathrin Neumann, Ralf S. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Lundin, Knut Erik Aslaksen Sollid, Ludvig M.
Pályázati támogatás:	120392 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM072049
Első szerző:	Iversen, Rasmus
Cím:	Strong Clonal Relatedness between Serum and Gut IgA despite Different Plasma Cell Origins / Iversen Rasmus, Snir Omri, Stensland Maria, Kroll José E., Steinsbø Øyvind, Korponay-Szabó Ilma R., Lundin Knut E. A., de Souza Gustavo A., Sollid Ludvig M.
Dátum:	2017
ISSN:	2211-1247
Megjegyzések:	Mucosal antigens induce generation of lamina propria plasma cells (PCs) that secrete dimeric immunoglobulin A (IgA) destined for transport across the epithelium. In addition, blood contains monomeric IgA. To study the relationship between mucosal and systemic antibody responses, we took advantage of celiac disease patient samples for isolation of gut PCs as well as serum IgA and IgG reactive with a gluten-derived peptide or the autoantigen transglutaminase 2. Proteomic analysis of serum IgA revealed antigen-specific V-gene preferences, which matched those found in gut PCs. Further, gut PC CDR-H3 sequences were abundant in serum IgA but also detectable in serum IgG. Our data indicate that the same B cell clones that give rise to gut PCs also contribute to the serum antibody pool. However, serum IgA antibodies had a molecular composition distinct from that of IgA antibodies secreted in the gut, suggesting that individual B cell clones give rise to different PC populations.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban celiac
Megjelenés:	Cell Reports 20 : 10 (2017), p. 2357-2367. -
További szerzők:	Snir, Omri Stensland, Maria Kroll, José E. Steinsbø, Øyvind Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Lundin, Knut Erik Aslaksen de Souza, Gustavo A. Sollid, Ludvig M.
Pályázati támogatás:	OTKA-101788 OTKA FP6-2005-FOOD-4B-36383) Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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