Studies on mice showed that chitosan as an adjuvant for H5 inactivated influenza vaccines administered intramuscularly enhances significantly antibody titers and protective efficiency not only against homologous influenza viruses, but also against drift variants. Chitosan adjuvanted vaccines induced high antibody titers after a single immunization and with a low dose of antigen. High antibody titers remained for at least 6 months. Chitosan adjuvanted vaccine stored at 4 degrees C preserves its adjuvant properties for at least 8 months. Chitosan stimulates proliferative and cytotoxic activity of splenic mononuclear leukocytes in mice and promotes an increase in the numbers of CD3, CD3/NK, I-AK (MHC II), and H-2Db (MHC I) cells. After intramuscular immunization, chitosan did not induce IgE antibodies and antibodies against chitosan itself. Chitosan is a promising adjuvant candidate for inactivated influenza vaccines administered parenterally.

IL-4 is a pleiotropic immunoregulatory cytokine secreted by Th2 subset of CD4(+) Th cells. Several transcription factors (TFs) have been determined with various degrees of certainty to bind the IL-4 promoter and to regulate its expression in human. To investigate the mechanisms responsible for phenotypic effects of the C-33T IL-4 promoter polymorphism, we performed a search of TFs binding to this promoter locus and discriminating the -33C and -33T alleles. In silico searches suggest few factors bind this region. Using an electromobility shift assay we found that Jurkat T cells contained proteins which specifically interacted with oligonucleotide probes, corresponding to the -33 region. Considerable binding differences between C and T alleles were demonstrated using competitive conditions, the proteins bound predominantly with -33C allele. We found that the transcription factor Oct-1 produced the major shifted complex. The binding of Oct-1 was not improved using activated nuclear extracts; however, we observed increases in other shifted complexes upon cell activation. We suppose that Oct-1 occupancy may compete for binding of activator proteins to closely or overlapped binding sites. Our findings suggest that the interplay between Oct-1 and unknown TFs may be responsible for the C-33T polymorphism effects.

Aim of this research has been to create a method to detect sIgE to thyroid peroxidase (TPO) in serum of the patients with autoimmune and allergic diseases.Materials and methods. In this research native affine-purified TPO (more the 95% clean, enzyme activity 60±15 of enzyme unit per mg) with immune dominant elements only (confirmed by inhibitory ELISA) has been used. The detection of sIgE in serum, combined with TPO, was carried out with monoclonal antibodies to IgE (8E/4F4) conjugated with horseradish peroxidase.Results. In serum of patients with bronchial asthma, allergic rhinitis and chronic spontaneous urticarial sIgE to TPO has been detected in 18—21% of cases. The healthy people and the patients with autoimmune thyroiditis had no sign of sIgE to TPO in their serum.Conclusion. The detection of sIgE to TPO in cases of patients with chronic spontaneous urticarial and allergic diseases will make possible to perform the early diagnosis of thyroid autoimmune disorders and provide timely and adequate therapy.

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Background. To evaluate the impact of atopic reactivity in humoral immune response to H. pylori in children with gastroduodenal diseases. Materials and methods. In 69 children with gastroduodenal diseases and in 14 healthy people we revealed the total IgE level, IgM-, IgG-, IgA- and IgE-antibodies to H. pylori in serum samples, slgA in saliva and IgE- antibodies to H. pylori in supernatant samples of faeces with ELISA method. Results. Chronic gastritis/gastroduodenitis in children with allergy are associated with a lower frequency of detection of IgG-and IgA- antibodies to H. pylori as well as with lower level of slgA and elevated levels of total IgE и IgE- antibodies to H. pylori in sera. Conversely, non-atopic patients showed high levels of slgA and high frequency of detection of IgA- antibodies to H. pylori. 60% of non-atopic children with gastroduodenal ulcers had elevated total IgE level, but IgE level to H. pylori was low as well as in healthy control group. IgE antibodies to H. pylori were detected in 95-100% of supernatant samples of faeces in all groups of patients with the highest level of IgE antibodies in children with gastroduodenal ulcers. It was revealed the direct correlation between the IgE antibodies to H. pylori level in serum and in supernatant samples of faeces in atopic children. Conclusion. The elevation of IgE antibodies to H. pylori is a result of constitutive Th2 immune response which reflects the mechanisms of mucosal immune defense independently from associated atopic diseases.