Helicobacter pylori is a widely spread pathogenic microorganism. It penetrates the mucous tunic of the stomach and the duodenum and causes diseases in the gastrointestinal tract, including oncologic ones. This agent is able to be chronically persistent in a body and frequently there are no apparent symptoms of it; therefore, it is difficult to detect this pathogen in due time. Risk analysis related to occurrence and development of various pathologies associated with Helicobacter pylori, revealed that their clinical course was to a great extent determined by an immune response that emerged after infection. There are data that Helicobacter pylori is able to influence protective immune reactions making their balance to move to an increase in immune-suppressive components, for example, increased concentrations of T-regulatory cells and cytokines produced by them. However, some data can be found on Helicobacter pylori ability to induce anti-inflammatory responses which include those associated with T-helpers of the 1st and 17th types. Our research goal was to reveal peculiarities of effects produced by this pathogen on γ-interferon as one of basic products by 1st type T-helpers and on contents of the 17th type T-helpers determined as cells belonging to CD4 + CD161 + and CD4 + IL17 + phenotypes under direct contacts between bacteria and lymphocytes. Our research objects were clinical isolates of Helicobacter pylori and blood samples taken from people without helicobacter infection in their case history. We extracted lymphocytes with immunomagnetic separation out of mononuclear blood cells obtained via functioning in density gradient. Their concentrations were assessed with cytofluorometry; cytokines products, with enzyme-linked immunosorbent assay. We showed that CD4 + CD161 + and CD4 + IL17 + cells content didn't change when they were cultivated together for 18 hours under influence exerted by Helicobacter pylori, while products of γ-interferon increased considerably. It can probably be related to activation of the 1st type T-helpers under effects produced by direct contact with bacteria. However, we didn't detect any activation of the 17th type T-helpers. Therefore, we can assume that effects produced by Helicobacter pylori on T-helpers under direct contact cause a response in a form of the 1st type T-helpers activation.

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Estimating risks of infections induced by gram-negative Helicobacter pylori, is a vital problem for healthcare due to wide spread of the agent and wide range of induced pathologies which include malignant neoplasms in gastrointestinal tract. The agent is prone to long-term chronic persistence despite its "fragility" and its being greatly demanding to culturing conditions. The persistence issue is of special interest here as it is related to data on Helicobacter pylori capability to change immune response in infected people inducing suppressive regulatory immune reactions which are more favorable for the agent, both in stomach and in a whole body. Our research goal was to estimate Helicobacter pylori capability to induce differentiation of regulatory CD4+CD25+FoxP3+ human T-cells as basic mediators of immune response regulation under direct contact between bacteria and T-cells without any participation of most professional antigen-presenting cells. Our re- __________________________Ó Matveichev