The nonclassic clinical presentation of celiac disease (CD) becomes increasingly common in physician's daily practice, which requires an awareness of its many clinical faces with atypical, silent, and latent forms. Besides the common genetic background (HLA DQ2/DQ8) of the disease, other non-HLA genes are now notably reported with a probable association to atypical forms. The availability of high-sensitive and specific serologic tests such as antitissue transglutuminase, antiendomysium, and more recent antideamidated, gliadin peptide antibodies permits to efficiently uncover a large portion of the submerged CD iceberg, including individuals having conditions associated with a high risk of developing CD (type 1 diabetes, autoimmune diseases, Down syndrome, family history of CD, etc.), biologic abnormalities (iron deficiency anemia, abnormal transaminase levels, etc.), and extraintestinal symptoms (short stature, neuropsychiatric disorders, alopecia, dental enamel hypoplasia, recurrent aphtous stomatitis, etc.). Despite the therapeutic alternatives currently in developing, the strict adherence to a GFD remains the only effective and safe therapy for CD.
Breast cancer (BC) is the most common cancer in women worldwide, with 2.3 million cases recorded in 2020. Despite improvements in cancer treatment, patients with BC still succumb to the disease, due to regional and distant metastases when diagnosed at later stages. Several immune checkpoint inhibitors have been approved for BC treatment, based on their expression and role in maintaining immunosurveillance against tumors. The present study aimed to evaluate the expression of 12 immune checkpoints in patients with BC, and assess their role as diagnostic and therapeutic markers. Expression levels were measured using reverse transcription-quantitative polymerase chain reaction. Among the 12 immune markers, herpesvirus entry mediator (HVEM) was found to be significantly upregulated in patients with malignant BC compared to non-malignant controls, with a relative fold change (FC) of 1.46 and P=0.012. A similar finding was observed for cytotoxic T-lymphocyte-associated antigen 4 (CTLA4; FC=1.47 and P=0.035). In addition, receiver operating characteristic curve analysis revealed that HVEM expression allowed significant differentiation between groups, with an area under the curve of 0.74 (P=0.013). Upregulation in both HVEM and CTLA4 was revealed to be significantly associated with the human epidermal growth factor receptor-2 (HER2)-enriched phenotype (FC=3.53, P=0.009 and FC=5.98, P=0.002, respectively), while only HVEM was significantly associated with the triple-negative phenotype (FC=2.07, P=0.016). Furthermore, HVEM was significantly higher in patients with grade III tumors (FC=1.88, P=0.025) and negative vascular invasion (FC=1.67, P=0.046) compared with non-malignant controls. Serum protein levels were assessed by multiplex immunoassay, and a significant increase in HVEM was detected in patients with malignant BC compared with that in non-malignant controls (P=0.035). These data indicated that HVEM may serve as a potential biomarker and target for immunotherapy, especially for certain types of BC.
T HE current Study intends to study the mitochondrial genome proteins specifically focusing on the distribution of intrinsically disordered regions within these proteins. The UniProt were employed to obtain amino acid sequences of the mitochondrial proteins. Next, the obtained sequences were studied to identify their unique features. We used the PONDR VSL2 algorithm to assess the proteins for any order or disorder. According to study results, mitochondrial genome proteins were expected to depict unexpected levels of intrinsic disorder. The results also indicated the possibility of presence of 7 intrinsic disorder regions within these proteins. The disordered regions were mostly found to be associated with protein-protein interactions. The research indicated the presence of two to nine molecular recognition features in the assessed mitochondrial proteins. These features included short structure-prone segments, location of mitochondrial proteins inside long disordered regions and the feature of showing disorder-to-order transition during binding. Moreover, such regions were attributed with a number of sites characterized with posttranslational modifications. According to the analysis, there may be many disordered regions present within mitochondrial genome proteins leading to multifunctional nature of mitochondrial genome proteins in the signal transduction pathways where these proteins regulate the cell metabolism pathways.
This report provides a study on the ongoing infection, pathogenesis, and immunity of COVID-19. The study will also investigate the cytokine storm and the role of both dendritic cells and Natural Killer T cells, and will provide ample references for researchers who need immunological data on SARS-CoV-2. The review collects data from 60 different review and research articles. Viral antigens are predictable by the B cells or introduced to the T cells by MHC complexes, leading to the assembly of antibodies, magnified production of cytokines, and lysis during the acute stage of infection. In MHC, genetic polymorphism helps it to show a number of T lymphocyte epitopes over different MHCs. Their gene association and downregulated expression are related to the seriousness of COVID-19 and evaluated by special markers such as IL-1ra, MCP-3, IL-17, IP-10, GM-CSF, TNF, IL-10, IL-1β, and IL-6. Clinical researches have pointed out that both severe and mild forms of COVID-19 lead to changes in leukocyte subtypes and cytokine secretion. Not unexpectedly, treatments that concern immune response and curb the 2019 coronavirus cytokine storm (COVID-19) will increase the patients' chance to survive. Cytokine storm characteristics, coagulopathy, and alternative inflammatory consequences remain vague. New accurate medication techniques are often advanced by distinguishing shared or population-specific triggering and amplifying cytokines storm at a certain stage of COVID-19.
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