Central European Journal of Immunology最新文献

The use of Aquafilling can be associated with a variety of health complications. The filler is an inflammatory process trigger at the site of tissue contact. The aim of this study was to semiquantitatively compare the immunohistochemical expression of E-cadherin and N-cadherin in tissue material from two groups of patients. The first group underwent surgical removal of Aquafilling from the breast, while the second was subjected to breast augmentation with implants or breast lifts (control group). The study group consisted of tissue samples from 16 patients who had Aquafilling removed, while the control group comprised samples from 16 patients who underwent breast augmentation with implants or breast lifts. Histopathology, immunohistochemistry and morphometric analyses were performed, taking into account the number of immunopositive cells and also the immunohistochemical reaction area for E-cadherin and N-cadherin. There were significantly more immunopositive N-cadherin cells in both groups. The immunohistochemical reaction area for N-cadherin did not differ between the two groups. However, the immunohistochemical reaction area for E-cadherin was significantly larger in the test group than in the control group. Moreover, the reaction area for N-cadherin was significantly smaller than that for E-cadherin. In the control group, no significant differences were detected between the immunohistochemical reaction area for N-cadherin and E-cadherin. Immunohistochemical evaluation of N-cadherin and E-cadherin tissue expression may be useful in assessing early cell junction changes. Furthermore, semiquantitative morphometric analysis allows these alterations to be more precisely determined.

Introduction: Graves' orbitopathy (GO) is a common autoimmune disease, but its specific pathogenesis has not been fully elucidated. MicroRNAs (miRNAs) possess an important regulatory function in the occurrence and development of autoimmune diseases. In the present study, we explored the potential role of miR-182 in the diagnosis of GO.

Material and methods: The expression of miR-182, thyrotropin receptor (TSHR) and adipocytokines was ascertained by qRT-PCR assay. The triglyceride (TG) content was ascertained by ELISA assay. The lipid droplet content was identified by Oil Red O staining. The relationship between E74-like factor 3 (ELF3), miR-182 and TSHR was confirmed by ChIP, dual-luciferase reporter assay and RIP.

Results: The expression of miR-182 decreased, while TSHR increased, and adipocytokine (adiponectin, leptin, PPAR-γ, and AP2) levels were upregulated in preorbital adipose tissue of patients with GO and differential medium induced (DM-induced) 3T3-L1 cells. MiR-182 mimics inhibited adipocytokine expression, TG content and lipid droplets; however, miR-182 inhibitor had the opposite results. TSHR was a target gene of miR-182, and TSHR overexpression (oe-TSHR) reversed the effect of miR-182 mimics on adipogenic differentiation of 3T3-L1 by DM treatment. ELF3 transcription promoted miR-182 expression. Oe-ELF3 inhibited adipocytokine expression and reduced TG content and lipid droplets in DM-induced 3T3-L1 cells. MiR-182 inhibitor reversed the effect of oe-ELF3 on adipogenic differentiation in 3T3-L1.

Conclusions: ELF3/miR-182/TSHR axis alleviated Graves' orbitopathy by inhibiting adipogenic differentiation.

Introduction: Recurrent infections are important problems in syndromic patients. This study aimed to evaluate immunological abnormalities in patients who presented with recurrent infections and were diagnosed with rare syndromes.

Material and methods: This retrospective analysis included 14 patients with complaints of recurrent infections, all of whom were diagnosed with a rare syndrome.

Results: The study group consisted of patients with Aicardi syndrome, Brugada syndrome, Phelan- McDermid syndrome, trichothiodystrophy, LEOPARD syndrome, Prader-Willi syndrome, Seckel syndrome, trisomy 18 (Edwards' syndrome), Wiedemann-Steiner syndrome, West syndrome, Williams syndrome, 47,XYY syndrome, 16p13 deletion syndrome, and 13q1.3 deletion syndrome. Seven patients (50%) were girls and seven (50%) were boys (mean age, 56.7 ±32.9 months; median [range] age: 45.5 [27-153] months). There were high rates of consanguinity (50%), cesarean section delivery (71%), and hospitalization in the intensive care unit (78.5%). No patients had a family history of immunodeficiency. On admission, all patients exhibited humoral and/or cellular immune system abnormalities. During the follow-up period, all T-cell abnormalities were improved after immunoglobulin replacement therapy (IGRT), while B-cell abnormalities persisted. These findings suggested that the patients predominantly had antibody deficiencies associated with mild T-cell abnormalities because of recurrent infections. The rates of infections and hospitalizations were significantly reduced after IGRT (p < 0.001); the rate of intensive care unit admission also significantly decreased (from 78.5% to 21.4%). Two of the three oxygen-dependent patients exhibited improvement therein. IGRT was discontinued in two patients with significant clinical improvement during follow-up.

Conclusions: An immunological evaluation should be considered in pediatric patients with rare syndromes and recurrent infections. IGRT may help to improve the prognoses of these patients.

Triggering receptor expressed on myeloid cell-2 (TREM2) is a transmembrane receptor which is specifically expressed on myeloid cells. To date, TREM2 has been confirmed as a key factor in many pathologies, such as Alzheimer's disease, obesity-related metabolic syndrome, fatty liver and atherosclerosis. However, the role of TREM2 in tumors remains poorly understood. TREM2 is highly expressed in more than 200 primary and metastatic tumors, a feature that makes TREM2 a potential clinical target for tumor immunotherapy. The tumor microenvironment (TME) is the "soil" which tumors survive on and exhibits immunosuppressive characteristics. During the development of a tumor, TME will secrete various chemotactic factors to recruit myeloid cells. It is clear now that cancer progression and metastasis depend on the interactions between cancer cells and myeloid cell infiltration in TME. As an important receptor involved in inflammatory suppression signaling pathways, TREM2 may play an important role in immune escape by the tumor. Recently, several studies have illustrated that TREM2 expressed on tumor infiltrated myeloid cells acts as a crucial regulator of the antitumor immune response. In this review, we systematically summarize recent publications about the latest advances in knowledge of TREM2 in cancer, especially focusing on its role in tumor associated myeloid cells and tumor immunotherapy.

Several studies have implicated β2-microglobulin (B2M) in osteoarthritis (OA) pathology. Of the main constituents of synovial tissue, synovial fibroblasts and macrophages, the latter play a pivotal role in inflammation. Although several studies have investigated the effects of B2M on synovial fibroblasts, few have examined the impact on synovial macrophages. Here, we investigated the effect of B2M on the expression profiles of inflammatory cytokines and matrix metalloproteases (MMPs) in synovial macrophages. Synovial macrophages were isolated from the osteoarthritic synovium using an anti-CD14 anti- body and magnetic isolation system. Synovial macrophages were stimulated with B2M for 6 and 24 h. Following stimulation, cell surface marker (CD80, CD163, CD206), cytokine [interleukin (IL)-6, IL-8, tumor necrosis factor α (TNF-α)] and matrix metalloprotease (MMP; MMP-9 and MMP-13) genes were evaluated by real-time PCR. Additionally, cytokine concentrations in cell culture supernatant were determined using enzyme-linked immunosorbent assay (ELISA). B2M significantly increased CD80 and decreased CD163 expression. In addition, B2M stimulation increased inflammatory cytokines at both the mRNA and protein levels. While B2M likewise elevated MMP-13 levels, there was no difference in MMP-9 expression between vehicle and B2M-treated cells. B2M increased M1 macrophage marker, inflammatory cytokine, and MMP-13 expression in synovial macrophages. B2M-related activation of synovial macrophages may thus be associated with OA pathology.

The number of argyrophilic nucleolus organizer regions (AgNOR) is related to the proliferative activity of cells and the degree of neoplastic transformation. The surface area of AgNOR depending on nuclear structure may be a predictor of tumor recurrence, while research into acute leukemias is scarce. The aim of the study was to determine whether the assessment of AgNOR parameters is useful in the differentiation of acute leukemias and, together with cytogenetic changes, would allow for a quick evaluation of the risk group. The AgNOR structures were analyzed in terms of the shape, surface area and distribution in bone marrow blast cells in patients with acute leukemias. We observed significant differences in the AgNOR structures, simple, compound and complex patterns between acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Complex structures were more numerous in ALL than in AML patients. There were significant differences in the distribution of AgNOR configuration among various cytogenetic AML risk groups. We observed a significant difference in the mean number of AgNOR between ALL-T and ALL-B. We detected diversity in the AgNOR structures and pattern map in AML and ALL. Thus, presentation of a variety of AgNOR configurations is innovative and can be a useful method of differentiating patients with acute leukemia types and cytogenetic risk.

Dendritic cell (DC)-based immunotherapies have been utilized for the treatment of numerous diseases. However, the conventional generation strategies of DCs in vitro require 7 days and these DCs showed an unsatisfactory function, which prompted us to explore new approaches. We found that in vitro culture of human CD14⁺ cells, in the medium containing granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-4, as well as interferon β (IFN-β) for 48 h, followed by the maturation stimuli of IL-1β and poly I:C for another 24 h can be differentiated into high cross-presentation ability DCs (G4B-DCs). These DCs express high levels of CD11c, CD86, and HLA-DR, producing a high level of tumor necrosis factor α (TNF-α). Of note, compared with the conventional DCs, G4B-DCs showed a higher ability to promote allogeneic naïve CD4⁺ T cell and CD8⁺ T cell proliferation and interferon (IFN)-γ production. These DCs also have the remarkable ability to induce Flu-M1-specific CD8⁺ T cells. In addition, we found that these G4B-DCs express partially the cDC1 phenotype. These data indicate that G4B-DC is unique and may provide a relatively rapid alternative method for potential clinical use.

Introduction: The aim of the study was to assess the epidemic situation among veterinarians of the Świętokrzyskie Voivodeship, Poland, in relation to the control group.

Material and methods: The research was divided into 3 stages. Stage I involved the selection of subjects. In stage II, flow cytometry for immunophenotyping was performed and the percentage of the sub-population of CD4 cells and CD8 cells was assessed. Stage III involved collection of nasopharyngeal swab samples in order to determine the canine coronavirus CR-CoV mRNA with the rT-PCR method.

Results: The percentage of the CD4 and CD8 lymphocyte subpopulation in relation to the total lymphocyte population in veterinarians did not differ statistically from the percentage in the control group. The CD4/CD8 ratio in the group of veterinarians was on average 1.93, and 2.04 in the control group. There was no statistically significant difference between the groups, p = 0.591. Canine CR-CoV mRNA was not detected in any of the veterinarians or in the control group.

Conclusions: None of the veterinarians had a significant increase in T lymphocytes, which could be an effective defense against SARS-CoV-2.

Neonatal screening for inborn errors of immunity (IEI), based on quantification of T-cell-receptor- excision circles (TRECs) and kappa-deleting recombination-excision circles (KRECs) from dried blood spots (DBS), allows early diagnosis and improved outcomes for the affected children. Determination of TREC/KREC levels from prospectively collected newborns' Guthrie cards and from DBS samples of patients with confirmed IEI was done using a commercial kit. Retrospective assessment of flow cytometry evaluation of TREC/KREC correspondence with lymphocyte subpopulations and evaluation of the correlations between TREC and KREC with immune cells, based on the data from patients with suspected or confirmed immune disorders, were conducted. 2,228 Guthrie cards were tested, 1276 for TREC only and 952 for both TREC and KREC. Eight newborns (0.36%) were TREC positive and 10 (1.05%) had KREC below the cut-off. The re-testing rate was 1.88%. Retrospective analysis demonstrated that the TREC/KREC assay identifies 100% of severe combined immune deficiencies (SCID) cases when DBS were collected at birth. Correlation analysis showed moderate significant correlations between TREC and the absolute numbers of CD4 cells (r = 0.634, p < 0.01) and total T cells (r = 0.536, p < 0.01). The ability of KREC levels to predict abnormal absolute (AUC of 0.772) and relative (AUC 0.731) levels of B cells was demonstrated.

Introduction: Immunoglobulin A nephropathy (IgAN) is the most common glomerular disease worldwide, with a poor prognosis. The aim of our study was to identify key biomarkers and their associations with immune cells to aid in the study of IgAN pathology and immunotherapy.

Material and methods: The data of IgAN were downloaded from a public database. The metaMA package and limma package were used to identify differentially expressed mRNAs (DEmRNAs) and differentially expressed miRNAs (DEmiRNAs), respectively. Biological functions of the DEmRNAs were analyzed. Machine learning was used to screen the mRNA biomarkers of IgAN. Pearson's correlation coefficient was used to analyze the correlation between mRNA biomarkers, immune cells and signaling pathways. Moreover, we constructed a miRNAs-mRNAs targeted regulatory network. Finally, we performed in vitro validation of the identified miRNAs and mRNAs.

Results: 1205 DEmRNAs and 125 DEmiRNAs were identified. In gene set enrichment analysis (GSEA), tumor necrosis factor α (TNF-α) signaling via nuclear factor κB (NF-κB), apoptosis and MTORC-1 signaling were inhibited in IgAN. 8 mRNA biomarkers were screened by machine learning. In addition, the distribution of 8 immune cell types was found to be significantly different between normal controls and IgAN by difference analysis. Pearson correlation coefficient analysis demonstrated that AKAP8L was significantly negatively correlated with CD4⁺ memory T-cells. AKAP8L was also significantly negatively correlated with TNF-α signaling via NF-κB, apoptosis, and MTORC-1 signaling. Subsequently, 5 mRNA biomarkers predicted corresponding negative regulatory miRNAs.

Conclusions: The identification of 8 important biomarkers and their correlation with immune cells and biological signaling pathways provides new ideas for further study of IgAN.