Evidence indicates that lung cancer development is a complex process that involves interactions between tumor cells, stromal fibroblasts, and immune cells. Tumor-infiltrating immune cells play a significant role in the promotion or inhibition of tumor growth. As an integral component of the tumor microenvironment, tumor-infiltrating B lymphocytes (TIBs) exist in all stages of cancer and play important roles in shaping tumor development. Here, we review recent clinical and preclinical studies that outline the role of TIBs in lung cancer development, assess their prognostic significance, and explore the potential benefit of B cell-based immunotherapy for lung cancer treatment.

Though immune checkpoint blockade (ICB) against PD-1 has shown success in the treatment of lung cancer, not all patients respond. We have previously shown that adoptive transfer of double negative T (DNT) cells expanded from healthy donors can target leukemia but their role in treating established lung cancer is not clear. Here we explore the role of human DNT cells in targeting late-stage established lung cancer either alone or in combination with Nivolumab (anti-PD-1 antibody) and describe underlying mechanisms. DNT cells from resected lung cancer tissue of patients were analyzed by flow cytometry to determine their infiltration and PD-1 expression. Expansion capacity and anti-tumor function of lung cancer patient and healthy donor DNT cells were compared. Late-stage lung cancer xenograft models were developed to determine the anti-tumor effect of DNT cells alone or in combination with anti-PD-1 antibody, and the level of tumor-infiltrating DNT cells was quantified by histology and characterized by flow cytometry. Patient-derived tumor infiltrating lymphocytes contained a lower frequency of DNT cells with a higher expression of PD-1 relative to normal lung tissue. Ex vivo expanded patient- and healthy donor-derived DNT cells showed similar levels of cytotoxicity against lung cancer cells in vitro. Healthy donor-derived DNT cells significantly inhibited the growth of late-stage lung cancer xenografts, which was further augmented by anti-PD-1 through increased DNT cell tumor infiltration. This study supports the use of DNT cells for adoptive cellular therapy against lung cancer either alone or in combination with anti-PD-1.

Paraquat (PQ) is a widely used herbicide known to induce lung injury and fibrosis in humans. Naringin (Nar), a naturally occurring flavonoid, possesses anti-inflammatory and anti-fibrotic properties. This study explores the protective mechanisms of Nar against PQ-induced epithelial-mesenchymal transition (EMT) and pulmonary fibrosis, focusing on the N-Myc downstream-regulated gene 1 (NDRG1) and peroxisome proliferator-activated receptor gamma (PPARγ) signaling pathways. Results demonstrate that Nar treatment significantly suppresses the PQ-mediated increase in EMT and pro-fibrotic markers, such as TGF-β, Vimentin, Snail, N-cadherin, and α-SMA, while also reducing the release of pro-inflammatory and pro-fibrotic factors, including IL-6, TNF-α, IL-1β, TGF-β, and MMP-9. Additionally, Nar decreases NDRG1 levels and enhances PPARγ expression. Mechanistically, NDRG1 silencing led to diminished JNK activity, which restored PPARγ levels and alleviated the expression of EMT markers and cytochrome P450s (CYPs 1A2 and 2E1) in A549 cells. Furthermore, Nar effectively mitigated PQ-induced EMT, cellular migration, and invasion by downregulating NDRG1 and phosphorylated JNK while upregulating PPARγ. These findings highlight the critical involvement of the NDRG1/JNK/PPARγ signaling pathway in PQ-induced lung injury and suggest the therapeutic potential of Nar for pulmonary fibrosis.

Anti‐human globulin (AHG) reagents are widely applied in pretransfusion compatibility tests. The accuracy of detection with AHG reagents is mainly affected by irregular antibodies or cold agglutinins in blood samples, which are related to the human complement system. Although much has been written about various types and applications of AHG reagents, their characteristics, interference factors and optimal selection in pretransfusion compatibility tests still need to be further clarified. Here, we review clinical practice and basic studies that describe each AHG reagent, summarize the advantages and disadvantages of using different AHG reagents in the presence of cold agglutinins or complement‐fixing antibodies, explore the potential mechanisms by which the complement system influences detection with AHG reagents and address the question of how to optimally select AHG reagents for clinically significant antibody detection.

KANNO is a new human blood group that was recently discovered. The KANNO antigen shares the PRNP gene with the prion protein and the prion protein E219K polymorphism determines the presence or absence of the KANNO antigen and the development of anti-KANNO alloantibodies. These alloantibodies specifically react with prion proteins, which serve as substrates for conversion into pathological isoforms in some prion diseases and may serve as effective targets for resisting prion infection. These findings establish a potential link between the KANNO blood group and human prion disease via the prion protein E219K polymorphism. We reviewed the interesting correlation between the human PRNP gene’s E219K polymorphism and the prion proteins it expresses, as well as human red blood cell antigens. Based on the immune serological principles of human blood cells, the prion protein E219K polymorphism may serve as a foundation for earlier molecular diagnosis and future drug development for prion diseases.