Carbohydrate specificities of the murine DC-SIGN homologue mSIGNR1

C-type lectins are important receptors expressed by antigen presenting cells that are involved in cellular communications as well as in pathogen uptake. An important C-type lectin family is represented by DC-SIGN and its homologues in human and mouse. Here we have investigated the carbohydrate specificity of cellular mSIGNR1 and compared it with DC-SIGN and L-SIGN. mSIGNR1 has a similar specificity as human DC-SIGN for high mannose-containing ligands present on both cellular and pathogen ligands. However, the DC-SIGN molecules differ in their recognition of Lewis antigens; mSIGNR1 interacts not only with Le(x/y) and Le(a/b) antigens similar to DC-SIGN, but also with sialylated Lex, a ligand for selectins. The differential recognition of Lewis antigens suggests differences between mSIGNR1 and DC-SIGN in the recognition of cellular ligands and pathogens that express Lewis epitope

Long-term acid suppression by omeprazole in gastro-oesophageal reflux disease patients does not lead to anti-gastric autoantibody production

BACKGROUND: Helicobacter pylori-associated atrophy of the gastric corpus is associated with the presence of anti-canalicular autoantibodies. Also, long-term profound acid suppression in H. pylori-infected subjects may cause atrophic corpus gastritis. AIM: To investigate whether long-term acid suppression by omeprazole leads to antigastric autoantibodies. METHODS: Fifty patients, of which 34 H. pylori-positive on entry of the study, were treated with omeprazole (20-40 mg once daily) for reflux oesophagitis, and were evaluated for anti-gastric autoantibody responses by immunohistochemistry before and after treatment. H. pylori was not eradicated and patients were followed for an average of 6.6 years (range 3-14.1 years). In addition to immunohistochemistry, anti-H(+), K(+)-ATPase reactivity was assessed by Western blot in paired sera of 41 patients (26 H. pylori-positive and 15 uninfected) and results are critically evaluated. RESULTS: In immunohistochemistry, all patients were negative for anti-canalicular autoantibodies when omeprazole therapy started, except for two patients with corpus-predominant gastritis in the presence of H. pylori. One patient, who was H. pylori-negative, newly developed an anti-canalicular antibody response during therapy. CONCLUSIONS: Our results indicate that, as compared with non-infected patients, long-term profound acid suppression therapy in H. pylori-infected gastro-oesophageal reflux disease patients does not increase or accelerate gastric autoimmunit

Molecular specificity and functional properties of autoreactive T-cell response in human gastric autoimmunity

Human autoimmune gastritis (AIG) is a chronic inflammatory disorder of the gastric corpus. We have defined the antigen repertoire and the functional properties of in vivo activated CD