| First Author | Field J | Year | 2003 |
| Journal | Clin Immunol | Volume | 109 |
| Issue | 2 | Pages | 238-47 |
| PubMed ID | 14597223 | Mgi Jnum | J:109805 |
| Mgi Id | MGI:3629850 | Doi | 10.1016/s1521-6616(03)00225-0 |
| Citation | Field J, et al. (2003) Chemokine receptor CCR5 is not required for development of experimental autoimmune gastritis. Clin Immunol 109(2):238-47 |
| abstractText | 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. |
