Central European Journal of Immunology最新文献

Introduction: Polycomb repressive complex 1 (PRC1) is a crucial epigenetic modification complex that plays significant roles in embryonic development, cell differentiation, and tumorigenesis. However, its predictive value and role in immunotherapy remain unclear.

Material and methods: Expression of the PRC1 complex was analyzed through RNA-seq, quantitative PCR, and immunohistochemistry. Then, we utilized the TCGA and GEO databases to cross-validate the prognostic risk. A pan-cancer analysis was conducted, including clinical traits, tumor microenvironment (TME), tumor mutational burden (TMB), stemness indices, and drug sensitivity. Furthermore, we cross-validated the effect of PRC1 on immunotherapy through ROC Plotter and Kaplan-Meier Plotter databases. The immune cell infiltration and signaling pathways were further identified.

Results: The expression of PRC1 differed between tumor and normal tissue in most cases. In particular, the whole group exhibited consistent high abundance in gastric, colorectal, and liver cancer. In addition, the expression of PRC1 can serve as a marker of survival prognosis. The members of PRC1 were also associated with clinical characteristics, immune cell infiltration, immune checkpoint inhibitor (ICI)-related immune indexes, and drug sensitivity. Moreover, high expression of BMI1 can increase resistance to immunotherapy, with a worse prognosis. The expression level of BMI1 can affect the immune-related pathways, as indicated by the gene set enrichment analysis (GSEA).

Conclusions: Our study revealed the expression, prognostic value and mechanism of PRC1 in pan-cancer. Its core member BMI1 can be used as a biomarker for the prognosis of tumor patients and the efficacy of ICIs. It provides a theoretical basis for the implementation of individualized immunotherapy.

Introduction: The progression of fungal co-infection with COVID-19 depends on the patient's genetic innate immunity. Our goal is to understand the connection between the single nucleotide polymorphisms (SNPs) rs5743708 and rs16910526 in the toll-like receptor 2 (TLR2) and dectin-1 (CLEC7A) genes, respectively, and fungal infection in COVID-19 patients.

Material and methods: This study assessed the SNPs rs5743708 from the TLR2 gene and rs16910526 from dectin-1 by Sanger sequencing. Two groups of COVID-19 patients participated in this study: 110 COVID-19 patients free from fungal infection (COVID-19 FFI), and 77 COVID-19 patients with fungal infection (COVID-19 WFI).

Results: The AG genotype of the TLR2 SNP rs5743708 showed no significant association with fungal infection in COVID-19 compared to the AA genotype. However, the GG genotype and G allele were significantly associated with decreased vulnerability to fungal co-infections. Similarly, regarding the dectin-1 SNP rs16910526, the TG genotype did not show a significant association with fungal infection compared to the TT genotype, but the GG genotype and G allele were significantly related to decreased susceptibility to fungal co-infections in COVID-19. The TLR2 protein levels in the serum of COVID-19 patients with GG genotypes of TLR2 rs5743708 were elevated. Variations in the dectin-1 genotypes (specifically GG genotype) can also raise the levels of dectin-1 serum protein.

Conclusions: The relationship between TLR2 rs5743708 and dectin-1 rs16910526 SNPs and susceptibility to fungal infection in COVID-19 patients was found to be significant, highlighting the im- portance of investigating their connection to infection progression for personalized patient care. The variation in genotypes also affects the levels of corresponding serum TLR2 and dectin-1.

Introduction: Immune disorders, especially in individuals with humoral deficiencies, pose challenges during the COVID-19 pandemic. Vaccination efficacy in this population remains a critical concern amid circulating misinformation. This study aimed to analyse the post-COVID-19 vaccination immune response in individuals with immune disorders, focusing on humoral deficiency. The goal was to provide essential insights for tailored vaccination strategies.

Material and methods: Tests including Anti-SARS-CoV-2 QuantiVac ELISA, SARS-CoV-2 NeutraLISA, and Quan-T-Cell SARS-CoV-2 IGRA were conducted on 63 patients with humoral inborn errors of immunity. Statistical analysis employed descriptive statistics and visualizations.

Results: Patients exhibited diverse responses based on immunological diagnoses. Immunoglobulin G (IgG) antibody levels varied across disorders, with agammaglobulinaemia patients showing lower levels but positive interferon responses. IgG subclass deficiency patients demonstrated robust antibody and neutralizing responses. Other antibody production disorders displayed strong immune reactions. Common variable immunodeficiency patients, particularly adults, exhibited higher antibody levels, increased neutralization, and pronounced interferon responses compared to children.

Conclusions: This study underscores the nuanced immune responses in individuals with diverse immune disorders following COVID-19 vaccination. Insights into specific disorder-related variations provide a foundation for targeted vaccination approaches, contributing to enhanced protection in this vulnerable population.

Introduction: Modulating dendritic cells (DCs; inhibiting maturation and antigen-presenting capacity) potentially promote immune tolerance to the benefit of allografts. In this study, we aimed to elucidate the impact of miR-155 on DC maturation and allograft rejection.

Material and methods: Donor monkey bone marrow-derived dendritic cells (BMDCs) were transduced with anti-miR-155 lentivirus to inhibit miR-155 expression, and the T cell phenotype and function of DC^anti-155 upon lipopolysaccharide (LPS) stimulation were evaluated. In vivo, imDC, imDC^anti-NC, and imDC^anti-155 were injected into recipient monkeys before skin transplantation. The survival times of skin allografts were recorded and the proportions of T cell subsets in spleen and secretion levels of cytokines in serum were measured. SOCS1/JAK/STAT pathway expression was also examined.

Results: miR-155 level increased during the maturation of dendritic cells. Inhibition of miR-155 significantly attenuated LPS-induced DC maturation. imDC^anti-155 promoted the differentiation of regulatory T cells (Tregs) and augmented the secretion of immunosuppressive cytokines. In vivo, subcutaneous injection of imDC^anti-155 prolonged recipient monkey skin allograft survival times and attenuated immune rejection. An increase in the proportion of Treg cells and their secreted cytokines in serum was observed in the imDC^anti-155 group. Mechanistic insights suggest that miR-155 likely regulates the SOCS1-JAK/STAT pathway.

Conclusions: Suppression of miR-155 has the potential to inhibit DC maturation, affects the differentiation of T cell subsets, and prolongs skin allograft survival, which could serve as a promising therapeutic strategy for managing allograft rejection.