[Diagnosis of Helicobacter pylori infection: comparison with gold standard].

Marshall and Warren were the first to succeed in culturing Helicobacter pylori (H. pylori) from the gastric mucosa of patients with gastritis in 1983. H. pylori is a spiral-shaped bacterium that resides in the gastric mucosa and is one of the most common infections worldwide. H. pylori infection causes gastritis and peptic ulcers and is associated with the development of gastric cancer and MALT lymphoma. Now, a variety of accurate diagnostic tests are widely available. Both invasive tests (bacterial culture, histopathology, and RUT) and non-invasive tests (UBT and serological test) are conducted for the diagnosis of H. pylori infection. This review provides a general overview of the diagnostic methods and tests the characteristics (sensitivity and specificity) for H. pylori infection.

Blocking intrahepatic deletion of activated CD8+ T cells by an altered peptide ligand.

BACKGROUND: Activated CD8(+) T cells are retained by the healthy liver where the majority undergo apoptosis. The intrahepatic apoptosis of activated CD8(+) T cells is enhanced by the presence of SIINFEKL peptide. It is of great interest to identify strategies for maintaining intrahepatic T cell number and function in the presence of SIINFEKL peptides. AIM: Our aim was to test if low affinity peptides can block SIINFEKL peptide induced T cell deletion. METHODS: We used an in vivo model of intrahepatic CD8(+) T cell deletion with peptides of different affinities. RESULTS AND DISCUSSION: We show that the intrahepatic deletion of CD8(+) T cells by SIINFEKL peptide results in loss of in vivo cytotoxic T lymphocyte function. In contrast we show that a low affinity peptide (G4) does not result in intrahepatic deletion of CD8(+) T cells. High concentrations G4 peptide can however block intrahepatic deletion of activated CD8(+) T cells, and prevent loss of in vivo cytotoxicity due to SIINFEKL peptide. This is the first demonstration of blocking of SIINFEKL peptide induced CD8(+) T cell deletion in the liver, with enhancement of in vivo cytotoxicity.

Kupffer cells required for high affinity peptide-induced deletion, not retention, of activated CD8+ T cells by mouse liver.

The immune response to foreign antigens in the liver is often suboptimal and this is clinically relevant in chronic persistence of hepatotropic viruses. In chronic infection with the hepatitis C virus, activated CD8+ T cells specific for viral epitopes are present in the peripheral blood and the liver, yet viral clearance is unusual. To define the fate of activated CD8+ entering the liver, we developed a mouse model of portal vein injection of activated CD8+ T cells in vivo. Activated CD8+ T cells are retained very efficiently by the liver and undergo an approximately 8-fold expansion in the first 48 hours. This expansion is followed by apoptosis and a decline in numbers of the retained cells over the next 4 days. The presence of high affinity (HA) antigen does not affect the initial retention by the liver but greatly limits the expansion in the first 48 hours by increasing apoptosis of the retained cells. In the absence of Kupffer cells, the initial retention and expansion are unchanged, but HA antigen does not limit the expansion of the liver CD8+ T cell pool. In conclusion, these data identify a previously unknown phase of CD8+ T cell expansion after entering the liver, demonstrate that HA antigen limits the hepatic CD8+ T cell pool by inducing apoptosis, and that this effect requires Kupffer cells. Interfering with antigen presentation by Kupffer cells may be a strategy to limit HA antigen-induced deletion of activated CD8+ T cells entering the liver.