ROLE OF PURINE METABOLISM ENZYMES IN IMMUNE PATHOGENESIS OF FIBRO-CAVERNOUS PULMONARY TUBERCULOSIS
Emergence and development of pulmonary tuberculosis is often accompanied by the signs of immune system dysfunction. The key enzymes of purine metabolism, e.g., adenosine deaminase (ADA and its isoforms, i.e. ADA1, ADA1 protein complex, and ADA-2), ecto-5’-nucleotidase (5’-NC) controlling adenosine l...
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| Autores principales: | , , , |
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| Formato: | article |
| Lenguaje: | RU |
| Publicado: |
SPb RAACI
2016
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/ede457f9020c4ef6987dc344cc8ca773 |
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| Sumario: | Emergence and development of pulmonary tuberculosis is often accompanied by the signs of immune system dysfunction. The key enzymes of purine metabolism, e.g., adenosine deaminase (ADA and its isoforms, i.e. ADA1, ADA1 protein complex, and ADA-2), ecto-5’-nucleotidase (5’-NC) controlling adenosine levels, may play an important role in regulation of cell-mediated immunity. We have correlated the parameters of purine metabolism with cytokine production in patients with fibro-cavernous pulmonary tuberculosis (FCT) with a severe specific process. Our studies have revealed an association between cytokine production and purine metabolism indexes, thus reflecting an important role of the latters in immunopathogenesis of the hyperchronic specific disorder. It is mainly referred to adenosine deaminase (ADA1 and ADA2) which are antagonistic in regulation of IL-17 and IL-18. A significantly decreased activity of intracellular ADA1, lowered CD26 concentrations, with lacking intercorrelation, along with increased activity of ecto-ADA-2 is, generally, typical to patients with fibrous-cavernous tuberculosis, thus being a possible marker for prediction of unfavorable hyperchronic specific process, being consistent with functional depletion of immunocompetent cells. Lack of the ADA/ectopeptidase complexes leads to an imbalance between adenosine supply and its deamination. Increased extracellular adenosine concentrations in the patients with severe specific processes may cause metabolic alterations of immunocompetent cells, thus complicating clinical course of the disease, e.g., contributing to enhancement and progression of pulmonary fibrosis. |
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