RT Journal Article
T1 Experimental and genetic evidence for the impact of CD5 and CD6 expression and variation in inflammatory bowel disease.
A1 Casado-Llombart, Sergi
A1 Velasco-de Andres, Maria
A1 Catala, Cristina
A1 Leyton-Pereira, Alejandra
A1 Gutierrez-Cozar, Rebeca
A1 Suarez, Belen
A1 Armiger, Noelia
A1 Carreras, Esther
A1 Esteller, Miriam
A1 Ricart, Elena
A1 Ordas, Ingrid
A1 Gisbert, Javier P
A1 Chaparro, Maria
A1 Esteve, Maria
A1 Marquez, Lucia
A1 Busquets, David
A1 Iglesias, Eva
A1 Garcia-Planella, Esther
A1 Martin-Arranz, Maria Dolores
A1 Lohmann, Juliane
A1 Ayata, C Korcan
A1 Niess, Jan Hendrik
A1 Engel, Pablo
A1 Panes, Julian
A1 Salas, Azucena
A1 Domenech, Eugeni
A1 Lozano, Francisco
K1 CD5
K1 CD6
K1 Crohn’s disease
K1 inflammatory bowel disease
K1 ulcerative colitis
AB Crohn's disease (CD) and ulcerative colitis (UC) are inflammatory bowel diseases (IBD) resulting from the interaction of multiple environmental, genetic and immunological factors. CD5 and CD6 are paralogs encoding lymphocyte co-receptors involved in fine-tuning intracellular signals delivered upon antigen-specific recognition, microbial pattern recognition and cell adhesion. While CD5 and CD6 expression and variation is known to influence some immune-mediated inflammatory disorders, their role in IBD remains unclear. To this end, Cd5- and Cd6-deficient mice were subjected to dextran sulfate sodium (DSS)-induced colitis, the most widely used experimental animal model of IBD. The two mouse lines showed opposite results regarding body weight loss and disease activity index (DAI) changes following DSS-induced colitis, thus supporting Cd5 and Cd6 expression involvement in the pathophysiology of this experimental IBD model. Furthermore, DNA samples from IBD patients of the ENEIDA registry were used to test association of CD5 (rs2241002 and rs2229177) and CD6 (rs17824933, rs11230563, and rs12360861) single nucleotide polymorphisms with susceptibility and clinical parameters of CD (n=1352) and UC (n=1013). Generalized linear regression analyses showed association of CD5 variation with CD ileal location (rs2241002CC) and requirement of biological therapies (rs2241002C-rs2229177T haplotype), and with poor UC prognosis (rs2241002T-rs2229177T haplotype). Regarding CD6, association was observed with CD ileal location (rs17824933G) and poor prognosis (rs12360861G), and with left-sided or extensive UC, and absence of ankylosing spondylitis in IBD (rs17824933G). The present experimental and genetic evidence support a role for CD5 and CD6 expression and variation in IBD's clinical manifestations and therapeutic requirements, providing insight into its pathophysiology and broadening the relevance of both immunomodulatory receptors in immune-mediated disorders.
PB Frontiers Research Foundation
YR 2022
FD 2022-08-31
LK http://hdl.handle.net/10668/20591
UL http://hdl.handle.net/10668/20591
LA en
NO Casadó-Llombart S, Velasco-de Andrés M, Català C, Leyton-Pereira A, Gutiérrez-Cózar R, Suárez B, et al. Experimental and genetic evidence for the impact of CD5 and CD6 expression and variation in inflammatory bowel disease. Front Immunol. 2022 Sep 21;13:966184
DS RISalud
RD Apr 10, 2025