Патологическое течение противоинфекцион-ного иммунного ответа и клиническая манифе-стация инфекционного заболевания возникают при нарушениях иммунологической реактивности организма. В случае адекватного взаимодополня-ющего функционирования систем врожденного и адаптивного иммунитета, напротив, происхо-дит своевременное уничтожение любого инфек-ционного антигена (вне зависимости от пути его проникновения в макроорганизм) на уровне «первой линии защиты», как правило, в системе мукозального иммунитета, то есть иммунитета слизистых оболочек. При инфицировании чело-УДК 616.23/.24-002.2+616.248]-036. 65:615.357:616.2-008.87 DOI 10.20538/168265:615.357:616.2-008.87 DOI 10.20538/ -0363-2016 Для цитирования: Чурина Е.Г., Уразова О.И., Новицкий В.В., Есимова И.Е., Кононова Т.Е., Филинюк О.В., Колобов-никова Ю.В., Дмитриева А.И. Факторы дисрегуляции иммунного ответа (на различных ýтапах его реализации) при туберкулезе легких. Бюллетень сибирской медицины. 2016; 15 (5): 166-177 Факторы дисрегуляции иммунного ответа (на различных этапах его реализации) при туберкулезе легких Чурина Е.Г. Россия, 634050, г. Томск, пр. Ленина, 36 РЕЗЮМЕ В статье представлен обзор научных исследований, раскрывающих механизмы неэффективной реализа-ции антигенспецифического иммунного ответа при туберкулезе легких в зависимости от клинической формы (инфильтративный и диссеминированный туберкулез легких) и варианта течения (лекарствен-но-чувствительный и лекарственно-устойчивый туберкулез легких) заболевания. Установлено, что ме-ханизмы иммунного дисбаланса при туберкулезе легких связаны с нарушением костимуляции сигналов, необходимых для активации Т-лимфоцитов, и иммуносупрессорным действием регуляторных Т-клеток как при их взаимодействии с дендритными клетками на индуктивной стадии иммунного ответа, так и в процессе дифференцировки и пролиферации эффекторных клеток с формированием супрессорного режима иммунорегуляции.Ключевые слова: туберкулез легких, иммунный ответ, регуляторные Т-клетки, иммунорегуляция.* Чурина Елена Георгиевна, e-mail: Lena1236@yandex.ru века Mycobacterium tuberculosis (МВТ) развитие и прогрессирующее течение туберкулеза легких (ТЛ) практически всегда связано с наличием у пациента вторичной иммунологической недо-статочности [1][2][3]. С другой стороны, в основе любого иммунопатологического процесса лежит первичная активация иммунных реакций, однако в случае туберкулезного воспаления она носит кратковременный и неýффективный характер и не приводит к полноценной реализации много-стадийного иммунного ответа с образованием специфичных к антигену клеток памяти. Установ-лено, что механизм иммунного дисбаланса при туберкулезной инфекции связан, прежде всего, с поляризацией иммунного ответа в направле-нии Treg-и Th2-зависимых путей [4][5][6]. В свою очередь, избыточное количество регуляторных Толерогенные дендритные клетки: особенности цитокинового профиля и роль в нарушении инициации Т-клеточного иммунного ответа при туберкулезе легкихПрезентация антигена является ключевым ýта-пом иммунного ответа. Нарушение представления...
Aim. To study molecular genetic and morphological features of neoplasms in stomach and colon cancer associated with tissue eosinophilia. Methods. Study material was the tissue samples of malignant neoplasms of the stomach and colon obtained from the surgical procedures. Study groups were identified depending on the presence or absence of eosinophilic infiltration of the tumour tissue as well as on neoplasm localization. Medical records and outpatient patient cards were analyzed, presence of matastases in regional lymph nodes and grade of differentiation of malignant cells were evaluated. In tumour tissue expression of p53 and p21 proteins was evaluated by means of immunohistochemical technique. To study the distribution of polymorphic variants of р53 (G215C) and р21 (A1026G) genes, deoxyribonucleic acid extraction was performed from formalin-fixed and paraffin-embedded tissue samples obtained from the resection margins. Polymorphism genotyping of deoxyribonucleic acid samples was performed by restriction fragment length polymorphism analysis of amplification products with the use of polymerase chain reaction of specific genome regions with further visualization with ultraviolet light. Results. In patients with colon cancer associated with tissue eosinophilia tumour cells were shown to have higher grade of differentiation than in patients without eosinophilia. In stomach cancer associated with eosinophilic infiltration low expression of mutant p53 protein was revealed significantly more frequently as opposed to cancer without eosinophilia. Also in patients with stomach and colon cancer, association of tissue eosinophilia with carriage of G allele of р53 (G215C) gene polymorphism was found. Conclusion. Tissue eosinophilia in stomach and colon cancer is associated with favourable morphological cancer characteristics, low expression of mutant p53 protein and carriage of G allele of р53 (G215C) polymorphism.
Background: Gastric and colon tumors are often associated with eosinophilic infiltration of tumor tissue, the significance of which is still not entirely clear. The recruitment of eosinophils into the tissues can be in part regulated by galectins ― galactose-binding proteins which are expressed by a variety of tissues and are capable of exerting a broad range of effects. Aims: To evaluate the expression of galectin-1 and galectin-3 in tumor tissue, and gal-3 gene mRNA expression in blood eosinophils in patients with gastric and colon cancer with or without tissue eosinophilia. Materials and methods: The study included a total of 107 patients (84 males and 23 females, average age 60,9 6,8) with verified gastric cancer (52 persons) and colon cancer (55 persons), who underwent treatment or were registered at the dispensary at the regional medical institution Tomsk Regional Oncology Center (Tomsk, Russia). The control group consisted of 15 men and 11 women of comparable age. The materials of the research included samples of gastric and colon tumors obtained during surgery, and eosinophilic granulocytes isolated from whole blood by immunomagnetic separation. Galectin-1 and galectin-3 expression in tumor tissue was evaluated by immunohistochemistry. The expression of gal-3 gene mRNA in eosinophils was determined by real-time reverse transcription polymerase chain reaction. Statistical analysis of the results was carried out using the non-parametric Mann-Whitney U test for independent samples with Benjamini-Hochberg procedure for multiple comparisons, and the Chi-square Pearson criterion with Yates correction. Results: In patients with gastric cancer and colon cancer, regardless of the presence of tissue eosinophilia, low expression of galectin-3 in the tumor tissue and high expression of gal-3 gene mRNA in peripheral blood eosinophils were found. Gastric and colon cancer patients with eosinophilic infiltration of tumor tissue were characterized by low expression of galectin-1 within tumor cells (in 64.0% cases, 2 = 4.890, р = 0.029; and in 73.9% cases, 2 = 5.981, p = 0.031 respectively). There was a statistically significant connection between the level of galectin-1 expression by tumor cells and the presence of tissue eosinophilia both in gastric ( = 0.307) and colon cancer ( = 0.330). Conclusion: Low expression of galectin 1 and 3 by tumor cells in gastric and colon cancer with tissue eosinophilia indicates the lack of a significant effect of these proteins on the process of recruiting eosinophilic granulocytes into tumor tissue. Increased expression of galectin-3 in blood eosinophils in gastric and colon cancer is not associated with the presence of eosinophilic infiltration of tumor tissue.
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