These findings provide evidence of strong HHV-6 infection association with AIT development.

In this autopsy-based study, human herpesvirus-6 (HHV-6) and -7 (HHV-7) genomic sequence frequency, HHV-6 variants, HHV-6 load and the expression of HHV-6 antigens in brain samples from the individuals, with and without unspecified encephalopathy (controls), using nested and real-time polymerase chain reactions, restriction endonuclease, and immunohistochemical analysis were examined. GraphPad Prism 6.0 Mann-Whitney nonparametric and chi-square test and Fisher's exact test were used for statistical analysis. The encephalopathy diagnoses were shown by magnetic resonance imaging made during their lifetime and macro- and microscopically studied autopsy tissue materials. Widespread HHV-6 and/or HHV-7 positivity was detected in the brain tissue of various individuals with encephalopathy, as well as in controls (51/57, 89.4 % and 35/51, 68.6 %, respectively; p = 0.009). Significantly higher detection frequency of single HHV-6 and concurrent HHV-6 + HHV-7 DNA was found in pia mater meninges, frontal lobe, temporal lobe, and olfactory tract DNAs in individuals with encephalopathy compared to the control group. HHV-6 load and higher frequency of the viral load >10 copies/10(6) cells significantly differed in samples from individuals with and without encephalopathy. The expression of HHV-6 antigens was revealed in different neural cell types with strong predominance in the encephalopathy group. In all HHV-6-positive autopsy samples of individuals with and without encephalopathy, HHV-6B was revealed. Significantly higher detection frequency of beta-herpesvirus DNA, more often detected HHV-6 load >10 copies/10(6) cells, as well as the expression of HHV-6 antigens in different brain tissue samples from individuals with encephalopathy in comparison with control group indicate on potential involvement of these viruses in encephalopathy development.

Using a specific marker 1A4 (DAKO), a quantitative evaluation of alpha-smooth muscle actin (ASMA) in glomeruli has been performed on human renal biopsies from patients suffering from acute, postinfectious, endocapillary glomerulonephritis (GN; 9 biopsies), IgA nephropathy (11 biopsies) and membranoproliferative GN (11 biopsies) and appropriate controls expressing a very weak ASMA reactivity. A significantly increased expression was found in all categories of GN. The glomeruli from IgA nephropathy showed variation of ASMA expression (range 0.1-27.7%) and a pattern of ASMA staining that was mesangial, global and diffuse. This pattern was also seen in cases of IgA nephropathy with focal, segmental, proliferative GN. In all biopsies, the glomerular cell number and proliferation index was determined. All the categories of GN showed significantly increased glomerular cellularity and proliferation index. Among the three types of GN, the glomerular cellularity and proliferation was lowest in IgA nephropathy. The mean number of Ki-67-positive intraglomerular nuclei and the proliferation index were both significantly correlated with the mean number of glomerular cell nuclei. Morphometric estimates demonstrate increased ASMA expression in types of GN with different prognosis. This finding and the lack of correlation with proliferation markers together indicate that the role of ASMA in GN is complex. This method of ASMA estimation may be useful in further studies of its role in disease activity and prognosis.

Markedly increased deposition of collagen type VI takes place in renal fibrotic lesions. Simultaneously, interstitial fibrotic areas appeared to contain a great number of fibroblasts sharing morphological characteristics of classic fibroblasts and smooth muscle cells. Detailed examination of coexistence of these two interstitial phenomena should further clarify the cellular mechanisms involved in renal interstitial fibrosis.

T helper (Th) 17 cells and interleukin (IL)-17 play a significant role in the pathogenesis of autoimmune thyroid disease (AITD). However, it has recently become clear that Th17 cells are more heterogeneous and exhibit two different phenotypes, whereas IL-23 and IL-1β are crucial for the generation of pathogenic Th17 lymphocytes. We aimed to investigate the association between IL-17 and Th17-promoting cytokines in AITD by studying the immunoexpression patterns of IL-17, IL-23, and IL-1β in thyroid tissue. Following thyroidectomy, 29 patients with AITD (21 cases of Hashimoto's thyroiditis (HT) and 8 cases of Graves' disease (GD)) and 18 patients with colloid goiter, as controls, were enrolled in this study, and immunohistochemistry was performed. The expression level of IL-17 in thyrocytes was significantly higher in HT and GD patients than in colloid goiter patients. Immunopositivity for both IL-23 and IL-1β was significantly increased in HT patients compared to GD and colloid goiter patients. However, no difference was found between IL-23 or IL-1β expression in patients with GD and colloid goiter. A positive correlation between IL-17 and IL-23 as well as IL-17 and IL-1β expression was observed in HT patients (r = 0.574, p = 0.007 and r = 0.461, p = 0.036, respectively). In the GD group, IL-17 was positively correlated with IL-1β (r = 0.817, p = 0.013) but not with IL-23 expression. We found increased IL-23 and IL-1β expression in the HT group but not in the GD group. Furthermore, both interleukins were correlated with IL-17 immunopositivity in thyroid tissue, suggesting that pathogenic Th17-promoting cytokines may play a role in HT pathogenesis.