2024-03-28T06:36:33Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1165792017-06-13T06:57:03Zcom_10261_39com_10261_1col_10261_292
IL-6 promotes immune responses in human ulcerative colitis and induces a skin-homing phenotype in the dendritic cells and Tcells they stimulate
Bernardo, David
Vallejo-Díez, Sara
Mann, Elizabeth R.
Al-Hassi, Hafid O.
Martínez-Abad, Beatriz
Montalvillo, Enrique
Fernández-Salazar, Luis
Garrote, José Antonio
Arranz, Eduardo
Knight, Stella C.
European Commission
Junta de Castilla y León
St. Mark's Hospital Foundation
Brigid Balfour Fund
et al.
Dendritic cells (DCs) control the type and location of immune responses. Ulcerative colitis (UC) is considered a Th2 disease mediated by IL-13 where up to one third of patients can develop extraintestinal manifestations. Colonic biopsies from inflamed and noninflamed areas of UC patients were cultured in vitro and their supernatants were used to condition human blood enriched DCs from healthy controls. Levels of IL-13 in the culture supernatants were below the detection limit in most cases and the cytokine profile suggested a mixed profile rather than a Th2 cytokine profile. IL-6 was the predominant cytokine found in inflamed areas from UC patients and its concentration correlated with the Mayo endoscopic score for severity of disease. DCs conditioned with noninflamed culture supernatants acquired a regulatory phenotype with decreased stimulatory capacity. However, DCs conditioned with inflamed culture supernatants acquired a proinflammatory phenotype with increased expression of the skin-homing chemokine CCR8. These DCs did not have decreased T-cell stimulatory capacity and primed T cells with the skin-homing CLA molecule in an IL-6-dependent mechanism. Our results highlight the role of IL-6 in UC and question the concept of UC as a Th2 disease and the relevance of IL-13 in its etiology. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
This work was supported by Marie Curie Intra European Fellowship (FP7-people-IEF-2008-235993), St Mark’s Hospital Foundation, the Brigid Balfour Fund, and Junta de Castilla y León (GRS175/B/07).
Peer Reviewed
2015-06-15T10:21:19Z
2015-06-15T10:21:19Z
2012
2015-06-15T10:21:19Z
artículo
http://purl.org/coar/resource_type/c_6501
doi: 10.1002/eji.201142327
issn: 0014-2980
e-issn: 1521-4141
European Journal of Immunology 42(5): 1337-1353 (2012)
http://hdl.handle.net/10261/116579
10.1002/eji.201142327
http://dx.doi.org/10.13039/501100000780
http://dx.doi.org/10.13039/501100009491
http://dx.doi.org/10.13039/501100014180
#PLACEHOLDER_PARENT_METADATA_VALUE#
info:eu-repo/grantAgreement/EC/FP7/235993
Postprint
http://dx.doi.org/10.1002/eji.201142327
Sí
open
Wiley-VCH