CONTENTS OF IL-1Β, IL-RA, IL-4, IL-8 AND IFNΓ IN THE CHILDREN WITH MINOR CLINICAL FORMS OF TUBERCULOSIS INFECTED WITH TOXOPLASMA GONDII AND EPSTEIN–BARR VIRUS

• Main Authors: A. V. Kalityn, T. I. Dolgikh
• Format: Article
• Language: Russian
• Published: SPb RAACI 2014-07-01
• Series: Medicinskaâ Immunologiâ
• Subjects: cytokines; toxoplasmosis; epstein–barr virus; tuberculosis
• Online Access: https://www.mimmun.ru/mimmun/article/view/171

Abstract. A group of 122 children, aged 7 to 16 year, with minor clinical forms of tuberculosis and infected with Toxoplasma gondii (T. gondii) and Epstein–Barr virus (EBV) was examined to evaluate the cytokine system. Immunoenzyme techniques were used to detect the presence IgM, IgA, IgG to T. gondii and EBV, as well as IL-1β, IL-1Ra, IL-4, IL-8, and IFNγ cytokines in blood. The patients were classified into three groups: (I) children with IgG to T. gondii, (II) children with IgM or IgA to T. gondii (active toxoplasmosis), (III) children with T. gondii-specific IgA and EBV-IgG-EA (active course of both toxoplasmosis and EBV infection). A comparison group (IV) consisted of TB-infected, T. gondii-seronegative patients without EBV-IgG-EA. A control group included thirty persons without evident disease. In groups I-III, a simultaneous and significant increase in IL-4 and spontaneous IFNγ contents was found, in comparison with controls. In group III, however, a 4-fold depression in IL-1β production was revealed against group IV, along with a 5.5-fold stimulation IFNγ production (as compared with controls). In groups I, II, IV, an inadequate hyperproduction of IL-1β and low IL-1Ra levels were shown. In the group III, a 3.4-fold and 5,5 fold IL-1Ra decrease were found, as compared, respectively, with group IV and control group. IL-8 content in groups I to III significantly exceeded control values (a 2.9 to 3-fold increase, with higher rates in group II). Hence, a direct inhibitory effect of EBV upon cell-mediated immunity should not be excluded under the conditions of TB-infection and active toxoplasmosis, thus further aggravating the immune dysfunction. (Med.Immunol., 2008, vol. 10, N 2-3, pp 273-276).