IgE-containing cells in gastric mucosa with and without Helicobacter pylori infection.

Gastric mucosa responds with inflammation to Helicobacter pylori (H. pylori) infection. While numerous reports have shown that the immune system produces specific IgG, IgA, and IgM isotype anti H.

Inhibition of IgE production by epsilon (epsilon) chain-specific antisense oligonucleotides (AOs) studied on human myeloma cell line U266 and peripheral blood mononuclear cells of a patient with hypereosinophilia.

Based on cDNA sequence data epsilon chain-specific antisense oligonucleotides were synthesized and checked on in vitro IgE production. Using peripheral blood cells from a hypereosinophilic patient and a human IgE myeloma cell line, U266, marked reduction of in vitro IgE production measured by PRIST was observed. The effect of epsilon antisenses proved to be isotype specific since IgG production by both peripheral blood cells and a lymphoma cell line, CESS, was not affected.

[Immune responses of IgG, IgA and anti-CagA IgG to Helicobacter pylori in dyspeptic and peptic ulcer patients].

The anti-H. pylori IgG, IgA, and anti CagA responses in dyspeptic patients have been evaluated. Of 481 patients 76% tested positive for IgG anti-H.

[Epidemiology of Helicobacter pylori infection in Hungary (comparative sero-epidemiologic study)].

In the last decade pathogenetical role of Helicobacter pylori infection has been proved in development of gastroduodenal alterations. DNA-RNA hybridisation and protein profile studies proved that Helicobacter pylori is an organism distinct from other bacteria. Therefore serology became a useful method to study the epidemiology of Helicobacter pylori infection in various populations.

Inhibition of antibody-dependent cellular cytotoxicity (ADCC) by normal and pathological sera from patients with advanced lung cancer.

An improved ADCC assay for the detection of cancer-associated serum blocking factors is described. Inhibition of ADCC by sera was performed without preincubation and washing of effector cells. Effects of individual susceptibility of normal effector cells to serum inhibitors and of the background inhibition by normal sera were also avoided.