Gene interactions and pathways from curated databases and text-mining

◀ Back to HNRNPF

CCR6 — HNRNPF

Text-mined interactions from Literome

Sato et al., J Immunol 2000 : Stimulation of mature DCs with TGF-beta 1 also enhanced TNF-alpha induced down-regulation of the expressions of CCR-1, CCR-3, CCR-5, CCR-6 , and CXCR-4, and chemotaxis to their respective ligands, while this stimulation suppressed TNF-alpha induced expression of CCR-7 and chemotactic migratory ability to MIP-3 beta
Le Borgne et al., Immunity 2006 : Recruitment of circulating DC precursors, including Gr1+ monocytes, precedes the sequential accumulation of CD11c+ MHC class II+ DCs in dermis and epithelium via a CCR6/CCL20 dependent mechanism
Salazar-Gonzalez et al., Immunity 2006 (Salmonella Infections) : Thus, CCR6 dependent regulation of DCs is responsible for localized T cell dependent defense against entero-invasive pathogens ... Thus, CCR6 dependent regulation of DCs is responsible for localized T cell dependent defense against entero-invasive pathogens
Phadke et al., Am J Respir Crit Care Med 2007 (Aspergillosis, Allergic Bronchopulmonary...) : In adoptive transfer experiments, however, DCs from CCR6-deficient donors showed lesser accumulation in the lungs of infected mice as compared with wild-type cells, and transfer of wild-type, but not CCR6-deficient , DCs resulted in attenuated severity of infection in CCR6-deficient recipients
Robays et al., J Immunol 2007 (Asthma) : Using this approach, we show that CCR2, but not CCR5 or CCR6 , directly controls the accumulation of DCs into allergic lungs
Dieu et al., J Exp Med 1998 : Finally, detection by in situ hybridization of MIP-3alpha mRNA only within inflamed epithelial crypts of tonsils, and of MIP-3beta mRNA specifically in T cell-rich areas, suggests a role for MIP-3alpha/CCR6 in recruitment of immature DCs at site of injury and for MIP-3beta/CCR7 in accumulation of antigen loaded mature DCs in T cell-rich areas