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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autoimmune Diseases / immunology*
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Autoimmune Diseases / pathology
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CCR5 Receptor Antagonists
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Chemokine CCL3
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Chemokine CCL4
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Chemokine CCL5 / immunology
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Chemokine CCL5 / metabolism
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Chemokine CCL5 / pharmacology
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Crosses, Genetic
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DNA / chemistry
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DNA / genetics
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Disease Models, Animal
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Female
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Fluorescent Antibody Technique, Indirect
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Gastritis / immunology*
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Gastritis / pathology
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H(+)-K(+)-Exchanging ATPase / immunology
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H(+)-K(+)-Exchanging ATPase / metabolism
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Macrophage Inflammatory Proteins / immunology
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Macrophage Inflammatory Proteins / metabolism
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Male
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C57BL
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Mice, Knockout
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Mice, Transgenic
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Parietal Cells, Gastric / immunology
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Receptors, CCR5 / immunology*
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Reverse Transcriptase Polymerase Chain Reaction
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Stomach / immunology
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Stomach / pathology
Substances
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CCR5 Receptor Antagonists
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Chemokine CCL3
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Chemokine CCL4
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Chemokine CCL5
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Macrophage Inflammatory Proteins
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RANTES, Met-
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Receptors, CCR5
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DNA
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H(+)-K(+)-Exchanging ATPase