Chemokine receptor CCR5 is not required for development of experimental autoimmune gastritis. Export

@article{Field_et_al03, abstract = {Experimental autoimmune gastritis (EAG) is a model of human autoimmune gastritis, the underlying cause of pernicious anaemia. It is characterised by gastric mononuclear cell infiltrates, destruction of parietal and zymogenic cells, and autoantibodies to parietal cell-associated H(+)/K(+) ATPase. Here, we have investigated the role of CCR5 in the development of EAG. We found that the development of EAG was not prevented in CCR5-deficient mice. Using reverse-transcriptase analysis of stomachs from normal and gastritic mice we found no difference in expression of CCR5 and its chemokine ligands MIP-1alpha, MIP-1beta, and RANTES. We also found that the CCR5 antagonist met-RANTES failed to prevent the development of EAG induced by neonatal thymectomy. These observations suggest that the CC chemokine receptor CCR5 is not essential for development of EAG.}, address = {Monash University, Department of Pathology and Immunology, Central and Eastern Clinical School, AMREP Commercial Road, Prahran, 3181 Victoria, Australia.}, author = {Field, J. and Marshall, A. C. and J Hertzog, P. and Wells, T. N. and Alderuccio, F. and Toh, B. H.}, citeulike-article-id = {3282767}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/14597223}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=14597223}, issn = {1521-6616}, journal = {Clinical immunology (Orlando, Fla.)}, keywords = {autoantibody, ccr5, pernicious\_anemia}, month = {November}, number = {2}, pages = {238--247}, posted-at = {2008-09-18 00:53:27}, priority = {2}, title = {Chemokine receptor CCR5 is not required for development of experimental autoimmune gastritis.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/14597223}, volume = {109}, year = {2003} }

TY - JOUR ID - Field_et_al03 L3 - citeulike-article-id:3282767 N2 - Experimental autoimmune gastritis (EAG) is a model of human autoimmune gastritis, the underlying cause of pernicious anaemia. It is characterised by gastric mononuclear cell infiltrates, destruction of parietal and zymogenic cells, and autoantibodies to parietal cell-associated H(+)/K(+) ATPase. Here, we have investigated the role of CCR5 in the development of EAG. We found that the development of EAG was not prevented in CCR5-deficient mice. Using reverse-transcriptase analysis of stomachs from normal and gastritic mice we found no difference in expression of CCR5 and its chemokine ligands MIP-1alpha, MIP-1beta, and RANTES. We also found that the CCR5 antagonist met-RANTES failed to prevent the development of EAG induced by neonatal thymectomy. These observations suggest that the CC chemokine receptor CCR5 is not essential for development of EAG. IS - 2 JF - Clinical immunology (Orlando, Fla.) SN - 1521-6616 AD - Monash University, Department of Pathology and Immunology, Central and Eastern Clinical School, AMREP Commercial Road, Prahran, 3181 Victoria, Australia. EP - 247 TI - Chemokine receptor CCR5 is not required for development of experimental autoimmune gastritis. VL - 109 SP - 238 KW - autoantibody KW - ccr5 KW - pernicious_anemia AU - Field, J AU - Marshall, AC AU - J Hertzog, P AU - Wells, TN AU - Alderuccio, F AU - Toh, BH PY - 2003/11// UR - http://view.ncbi.nlm.nih.gov/pubmed/14597223 ER -