Research progress of therapeutic effects and drug resistance of immunotherapy based on PD-1/PD-L1 blockade.

Information feedback of 18F-FDG PET/CT computer imaging combined with tumor markers on recurrence and metastasis of non-small cell lung cancer.

Objective To establish and verify the method for detecting the immune phenotype of peripheral blood T lymphocytes by cellular immune chip technology, analyze the immune status, and discuss its clinical diagnostic value of different populations in the Qingyuan area. Methods First, a cellular immune chip was used to detect the number of T lymphocyte subsets CD3+, CD4+, CD8+, and CD4/CD8, followed by evaluating the accuracy and precision through a comparison with flow cytometry. After passing the performance verification, a large-scale detection was performed by a cellular immune chip in 8389 cases. Immunochip technology detects the expression of T lymphocyte subsets and analyzes the differences in cellular immune function among people with physical examination, inflammation, and cancer, as well as different cancer types and in genders. Results The cell immunochip method and flow cytometry method have the same accuracy and precision in detecting specimens, and the former is fast and simple, and is suitable for clinical use; big data analysis is expected to establish a reference range for CD3+, CD4+, and CD8+ T cell counts in Qingyuan. There are statistical differences in CD3+, CD4+, CD8+ T cell counts in physical examination, inflammation and cancer populations; there are also certain differences in CD3+, CD4+, CD8+ T cell counts and CD4/CD8 ratios between different cancer types and different diseases. Conclusion The method of cell immunochip technology to detect T lymphocyte subsets is simple and practical, with accurate results and rapid detection. It can be used for immune function monitoring and treatment prognosis evaluation of people with different diseases, and it is worthy of popularization and application in clinical practice.

Establishment and Clinical Application of a Method for Detecting T Lymphocyte Subsets by Cellular Immunochip Technology

Programmed cell death 1 (PD-1), a key immune checkpoint receptor, has been extensively studied for its role in regulating immune responses in cancer. However, recent research has unveiled a complex and dual role for PD-1 in tumorigenesis. While PD-1 is traditionally associated with immune cells, this article explores its expression in various cancer cells and its impact on cancer progression. PD-1's functions extend beyond immune regulation, as it has been found to both promote and suppress tumor growth, depending on the cancer type. These findings have significant implications for the future of cancer treatment and our understanding of the immune response in the context of cancer. This article calls for further research into the multifaceted roles of PD-1 to optimize its therapeutic potential and improve patient outcomes in the fight against cancer.

Multifaceted roles of PD-1 in tumorigenesis: From immune checkpoint to tumor cell-intrinsic function.

Influenza A virus (IAV) causes significant morbidity and mortality worldwide due to seasonal epidemics and periodic pandemics. The antigenic drift/shift of IAV continually gives rise to new strains and subtypes, aiding IAV in circumventing previously established immunity. As a result, there has been substantial interest in developing a broadly protective IAV vaccine that induces, durable immunity against multiple IAVs. Previously, a polyanhydride nanoparticle-based vaccine or nanovaccine (IAV-nanovax) encapsulating H1N1 IAV antigens was reported, which induced pulmonary B and T cell immunity and resulted in cross-strain protection against IAV. A key feature of IAV-nanovax is its ability to easily incorporate diverse proteins/payloads, potentially increasing its ability to provide broad protection against IAV and/or other pathogens. Due to human susceptibility to both H1N1 and H3N2 IAV, several H3N2 nanovaccines were formulated herein with multiple IAV antigens to examine the "plug-and-play" nature of the polyanhydride nanovaccine platform and determine their ability to induce humoral and cellular immunity and broad-based protection similar to IAV-nanovax. The H3N2-based IAV nanovaccine formulations induced systemic and mucosal B cell responses which were associated with antigen-specific antibodies. Additionally, systemic and lung-tissue resident CD4 and CD8 T cell responses were enhanced post-vaccination. These immune responses corresponded with protection against both homologous and heterosubtypic IAV infection. Overall, these results demonstrate the plug-and-play nature of the polyanhydride nanovaccine platform and its ability to generate immunity and protection against IAV utilizing diverse antigenic payloads. 

pdf/polyanhydride-nanovaccine-against-h3n2-influenza-a-virus-u16wyydfcq.pdf

Polyanhydride nanovaccine against H3N2 influenza A virus generates mucosal resident and systemic immunity promoting protection

T cell lymphopenia was a significant characteristic of severe influenza infection and it was associated with the functional changes of T cells. It is necessary to clarify the T cells characteristics of kinetic changes and their correlation with disease severity.In a cohort of hospitalized influenza patients with varying degrees of severity, we characterized lymphocyte populations using flow cytometry.The numbers of cycling (Ki67+) T cells at the acute phase of severe influenza were higher, especially in the memory (CD45RO+) T cell subsets. T cells from hospitalized influenza patients also had significantly higher levels of the exhausted marker PD-1. Cycling status of T cells was associated with T cell activation during the acute phase of influenza infection. The recruitment of cycling and activated (CD38+HLA-DR+) CD8+ T cells subset is delayed in severe influenza patients.The increased numbers of cycling memory (Ki67+CD45RO+) T cells subsets and delayed kinetics of activated (CD38+HLA-DR+) CD8+ T cells, could serve as possible biological markers for disease severity. 

/pdf/cycling-and-activated-cd8-t-lymphocytes-and-their-1xqjracm.pdf

Cycling and activated CD8+ T lymphocytes and their association with disease severity in influenza patients

Background Resident phenotypic memory CD8+ T cells are crucial for immune defense against pathogens. However, little is known about the potential transitions and regulation mechanisms of their function after influenza virus infection and reinfection. In this study, we utilized integrated transcriptome data and in vivo experiments to investigate the key characteristics behind it. Methods Two single-cell RNA sequencing (scRNA-seq) datasets of lung CD8+ T cells and one RNA-seq dataset of lung tissue after infection or reinfection were included. After Seurat procedures classifying CD8+ T subsets, the scCODE algorithm was used to identify the differentially expressed genes for GSVA, GO, and KEGG pathway enrichment. Monocle 3 and CellChat were used to infer pseudotime cell trajectory and cell interactions. The ssGSEA method was used to estimate the relative proportions of immune cells. The findings were confirmed with a mouse model via flow cytometry and RT-PCR analysis. Results Our study refined the landscape of CD8+ T-cell subsets in the lung, showing that CD8+ Trm cells accumulated in the lung within 14 days after influenza infection. The classical CD8+ Trm cells co-expressed a high level of CD49a and even maintained 90 days after primary infection. The ratio of CD8+ Trm cells decreased 1 day after influenza reinfection, which may be parallel with their potential transition into effector types, as observed in trajectory inference analysis. KEGG analysis suggested that PD-L1 expression and PD-1 checkpoint pathway were upregulated in CD8+ Trm cells on day 14 after infection. GO and GSVA analyses revealed that PI3K-Akt-mTOR and type I interferon signaling pathways were enriched in CD8+ Tem and Trm cells after reinfection. Additionally, CCL signaling pathways were involved in cell interaction between CD8+ Trm cells and other cells, with Ccl4-Ccr5 and Ccl5-Ccr5 ligand/receptor pairs being important between CD8+ Trm and other memory subsets after infection and reinfection. Conclusion Our data suggest that resident memory CD8+ T cells with CD49a co-expression account for a large proportion after influenza infection, and they can be rapidly reactivated against reinfection. Function differences exist in CD8+ Trm and Tem cells after influenza infection and reinfection. Ccl5-Ccr5 ligand/receptor pair is important in cell interactions between CD8+ Trm and other subsets.

/pdf/comprehensive-immune-landscape-of-lung-resident-memory-cd8-t-2ig79tqd.pdf

Comprehensive immune landscape of lung-resident memory CD8+ T cells after influenza infection and reinfection in a mouse model

/pdf/cycling-and-activated-cd8-t-lymphocytes-and-their-2wah59zt.pdf

This study aimed to investigate the relationship between sleep disorders and lymphocyte subsets and cytokines in patients with lung cancer undergoing radiotherapy, and to establish a theoretical foundation for predicting sleep disorders and preventing interventions in radiotherapy in lung cancer patients. Ninety-two patients with lung cancer requiring radiotherapy were selected as the study subjects. The patients' demographic data and disease-related conditions were investigated. Their quality of sleep was measured before radiotherapy, after two and four weeks of radiotherapy, and at the end of radiotherapy. According to the Pittsburgh Sleep Quality Index Number Table (PSQI), patients with PSQI score> 7 points were put into a sleep disorder group, and patients with PSQI score 0-7 were put into a normal sleep group. Lymphocyte subsets were enumerated and cytokine levels (IL-6, IL-1b) were measured during these four periods. The difference in sleep disorders at four weeks between patients with or without synchronous chemotherapy was statistically significant (P less than 0.05). The levels of lymphocyte subsets in the sleep disorder group and the control sleep group showed no difference in the index of lymphocyte subsets before radiotherapy. In the sleep disorder group, CD4+ cells were lower after two weeks of radiotherapy (P less than 0.05). After four weeks of radiotherapy, CD3+, CD4+, and CD16+56+ subsets were lower (P less than 0.05). At the end of radiotherapy, there was no difference in each index. There was no significant difference in IL-6 levels between the two groups before radiotherapy, after two weeks, or after four weeks (P greater than 0.05). At the end of radiotherapy, IL-6 levels in the sleep disorder group were higher than those in the control sleep group (P less than 0.05). There was no significant difference in IL-1b between the two groups (P greater than 0.05). In conclusion, monitoring of T-lymphocyte subsets and IL-6 levels in patients is enhanced during radiotherapy. Clinically effective programs of radiotherapy for lung cancer improve the body's immune status.

Relationship between sleep disorders and lymphocyte subsets and cytokines in patients with lung cancer.

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Cycling and activated CD8+ T lymphocytes and their association with disease severity in influenza patients

Comprehensive immune landscape of lung-resident memory CD8+ T cells after influenza infection and reinfection in a mouse model

Cycling and activated CD8+ T lymphocytes and their association with disease severity in influenza patients

Relationship between sleep disorders and lymphocyte subsets and cytokines in patients with lung cancer.