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Immunophenotype of peripheral blood natural killer cells and IL ‐10 serum levels in relation to Helicobacter pylori status
Author(s) -
Rudnicka Karolina,
Matusiak Agnieszka,
Miszczyk Eliza,
Rudnicka Wiesława,
Tenderenda Michał,
Chmiela Magdalena
Publication year - 2013
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12120
Subject(s) - il 2 receptor , immunology , cd3 , biology , immunophenotyping , flow cytometry , immune system , cd16 , natural killer cell , lymphocyte , cytotoxic t cell , t cell , cd8 , in vitro , biochemistry
Recent findings suggest that NK (Natural Killer) cells may directly modulate the antimicrobial immune responses. In this study, we performed immunophenotypic analysis of peripheral blood NK cells with regard to CD 56, CD 16, Nkp46, and CD 25 markers, as well as IL ‐10 levels quantification in the sera samples of asymptomatic, H. pylori (Hp)‐infected or uninfected individuals, and combined these results with our previous findings on lymphocyte cytotoxic activity. Twenty healthy volunteers [10 Hp(−);10 Hp(+)] were included in the study. The percentages of classic lymphocytes ( CD 3 + ) and NK cells ( CD 3 − CD 56 + , CD 3 − Nkp46 + , CD 3 − CD 16 + ) with or without CD 25 receptor were evaluated by fluorochrome‐conjugated monoclonal antibody staining and flow cytometry analysis. IL ‐10 quantification was performed by enzyme‐linked immunosorbent assay‐ ELISA . Our study showed elevated levels of IL ‐10 and higher NK cell numbers of both CD 3 − CD 56 + CD 25 + and CD 3 − Nkp46 + CD 25 + phenotypes, as well as CD 3 + CD 25 + classic lymphocytes in Hp(+) compared with Hp(−) individuals. No differences between Hp(−) and Hp(+) individuals were found either in total number of classic lymphocytes or NK cell subtypes. Our data suggest that in Hp(+) donors, there is a domination of lymphocytes and NK cells co‐expressing CD 25 marker, which might be influenced by the regulatory IL ‐10. This phenomenon may be a result of H. pylori adaptation to a changing environment in vivo leading to a chronic infection and lack of severe gastric pathologies.

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