CUSABIO Semi-annual Literature Review: Consolidating 1500+ High Impact Factor Papers, Cumulative Impact Factor Exceeds 5000+!

The authors investigated the lung-resident B-cell responses in patients from the TRACERx 421 (Tracking Non-Small Cell Lung Cancer Evolution Through Therapy) and other lung cancer cohorts, as well as in a recently established mouse model of lung adenocarcinoma. They found that both human and mouse lung adenocarcinomas induce local germinal center reactions and tumor-binding antibodies, with the envelope glycoprotein of endogenous retroviruses (ERV) identified as the major target of anti-tumor antibodies.

Furthermore, the authors discovered that effective immunotherapy in the mouse model required the formation of TLS (tertiary lymphoid structures) dependent on CXCL13. Conversely, therapeutic treatment with CXCL13 enhanced anti-tumor immunity and synergized with ICB.

The findings of this study provide a potential mechanistic basis for the association between TLS and the immune therapy response.

The authors of this study have revealed the mechanisms underlying food immune tolerance. Previous research has mainly focused on the influence of commensal bacteria in the colon on immune tolerance, while less is known about the mechanisms of food immune tolerance. This study found that food antigens induce immune tolerance by maintaining regulatory T cells in the intestine. Additionally, food antigen-specific T cells exhibit a regulatory T cell subset that lacks inflammatory functions. In addition to the conventional antigen-presenting cells, intestinal epithelial cells (IECs) also shape the population of regulatory IL10+CD4+ T cells in the small intestine.

The authors of this study have elucidated the important role and mechanism of a long non-coding RNA (lncRNA) associated with inflammatory bowel disease (IBD), which is of significant importance for understanding the maintenance of intestinal homeostasis and the protection of the host against colitis. They have also described for the first time the involvement of the long non-coding RNA, named CARINH (Colitis-Associated Regulatory lncRNA), in protecting against inflammatory bowel disease.

The study reveals a unique positive feedback mechanism of protein expression regulation mediated by the ADD1/MATR3/ADAR1 axis. This process is termed "Protein-guided Editing of ADAR1 on its own mRNA (PEDORA)" and is proposed to constitute an additional layer of protein expression control. PEDORA may represent a yet undiscovered mechanism in the regulation of eukaryotic gene expression.

The authors demonstrated through lineage tracing experiments that a subset of Osr1-expressing cells represents mesenchymal LTo progenitor cells. By studying the heterogeneity of Osr1+ cells, distinct features of mesenchymal LTo cells from different anatomical locations were identified, and a shared precursor relationship between mesenchymal LTos and LN-associated adipose tissue was established.

This study redefines the roles and identities of mesenchymal tissue-forming cells and proposes a cooperative cellular functional model to reconcile current views on LN formation.

The study revealed that HLA-DP4-Ply427-441 plays a similar role on both private and public TCRs. These findings uncover the mechanistic determinants of nearly global immune responses focused on cross-border bacterial epitopes, which are of significant importance in devising complementary strategies against life-threatening infectious diseases, including invasive pneumococcal infections.

The authors utilized mass spectrometry (MS)-based proteomics approach to identify host proteins that interact with the RNA-dependent RNA polymerase (RdRp) non-structural protein 12 (nsp12) of SARS-CoV-2. Among the candidate factors, cyclin-dependent kinase 2 (CDK2), a member of the cyclin-dependent kinase family involved in cell cycle regulation, was found to interact with nsp12. This interaction led to phosphorylation of nsp12 at the T20 site, facilitating the assembly of the RdRp complex composed of nsp12, nsp7, and nsp8, and promoting efficient synthesis of viral RNA.

Sorbitol and pathogenic strains of Klebsiella play a significant role in the pathogenesis and epidemiology of Clostridioides difficile infection (CDI) in patients with inflammatory bowel disease (IBD).

This study has identified the important role of sorbitol and sorbitol metabolism in the pathogenesis and epidemiology of CDI in IBD patients. Therefore, by eliminating sorbitol from the diet or inhibiting host production of sorbitol, CDI in IBD patients can be prevented or improved.

The authors evaluated pIgR (polymeric immunoglobulin receptor) and IgA in the livers of patients with alcohol-related hepatitis and control groups. pIgR-deficient mice exhibited more severe liver damage, steatosis, and inflammation compared to wild-type mice after ethanol feeding. Additionally, pIgR-deficient mice showed increased plasma endotoxin levels and higher liver bacterial load, indicating increased bacterial translocation.

The study results suggest that dysfunction of liver pIgR, coupled with impaired antibacterial defense of IgA in the gut, contributes to the development of alcohol-related liver disease.

The authors found that APAP (acetaminophen) exposure is associated with specific alterations in the gut microbiota, including a significant reduction in Lactobacillus vaginalis. Mice receiving L. vaginalis demonstrated resistance to APAP-induced liver toxicity, which was attributed to the release of the isoflavone daidzin from the dietary source by bacterial β-glucosidase.

In APAP-exposed germ-free mice, the hepatoprotective effect of L. vaginalis was abolished by a β-glucosidase inhibitor. Similarly, L. vaginalis lacking β-glucosidase showed poorer outcomes in mice treated with APAP, but these differences could be overcome by the administration of daidzin from soybean.

Mechanistically, daidzin prevented ferroptosis, which was associated with reduced expression of farnesyl diphosphate synthase (Fdps). Fdps activates a key iron death pathway involving AKT-GSK3β-Nrf2.

Therefore, soybean-derived daidzin released by β-glucosidase of L. vaginalis inhibits Fdps-mediated ferroptosis in liver cells, providing a promising therapeutic approach for drug-induced liver injury.