responses in cells Research Articles (Page 1)

HIV virion capturing liposomes for therapeutic vaccination.

Pectolinarin alleviates inflammatory injury in a lipopolysaccharide-induced pneumonia model by inhibition of the TLR4/MyD88/NF-κB pathway.

Cellulose, the most abundant biopolymer on Earth, offers a sustainable alternative to synthetic materials in biomedical applications. Among cellulose-derived materials, nanocellulose has attracted increasing attention due to its favourable biocompatibility, versatility, and compatibility with advanced fabrication techniques such as electrospinning, 3D printing, and freeze-drying. In this study, Polystyrene/nanocellulose composite membranes fabricated via electrospinning were produced and systematically characterized, and their cytocompatibility was comparatively evaluated against solvent-cast nanocellulose membranes and standard tissue culture plates. Comprehensive morphological and physicochemical analyses were performed, followed by cytocompatibility evaluations using primary human umbilical vein endothelial cells (HUVECs). Cell viability, proliferation, inflammatory response, and qualitative endothelial layer formation were evaluated over a 21-day culture period. HUVEC proliferation and viability on electrospun membranes were comparable to those observed on solvent-cast nanocellulose membranes and standard tissue culture plates (TCP) after 21days. All membrane formulations exhibited a reduction in reactive oxygen species over time, while electrospun membranes demonstrated a more homogenous cytokine expression profile (IL-6, IL-23, IFN-α2, and TNF-α) during long-term culture. However, qualitative assessment of endothelial layer formation indicated a delayed development of a mature endothelial monolayer on electrospun membranes compared with solvent cast membranes and tissue culture controls. Overall, these findings demonstrate the cytocompatibility of electrospun nanocellulose composite membranes and highlight how differences in fabrication strategy and resulting membrane characteristics influence endothelial cell responses. This study provides a comparative and exploratory evaluation of nanocellulose composite membrane systems, supporting their further consideration as sustainable biomaterial for vascular-related biomedical research.

The mechanosensitive ion channel Piezo1 promotes colitis by modulating oxidative stress and ferroptosis-related markers.

A specific integrin αPS3βPS1 heterodimer is required for hemocyte phagocytosis in Chinese mitten crab, Eriocheir sinensis.

Oral immunization with recombinant Lactococcus lactis expressing VP3 and VP3-IFNα fusion protein protects ducklings against novel goose parvovirus infection.

A self-assembled protein nanocage as a universal influenza vaccine induces enhanced broadly cross-reactive immunity.

Amplified ferroptosis and immunomodulation triggered by NIR-II photothermal-controllable CRISPR/Cas9 nanoplatform to treat osteosarcoma and prevent postsurgical implant-associated infections.

Prophylaxis Guided by CMV-Specific T-Cell Immunity in Lung Transplant Recipients: Prospective Interventional Study

Safety of in vivo gene therapy in children: mechanisms and management of liver injury.

Fc receptor-like (FCRL) proteins constitute a receptor family that displays overlapping yet distinct features compared to classical Fc receptors. In a healthy immune system, FCRL proteins play a role in promoting and regulating the immune response through their immunoreceptor tyrosine-based motifs. FCRL proteins are expressed mainly by B cells, suggesting a primary role in B-cell responses. For several autoimmune diseases, studies have shown that particularly FCRL4, which binds to dimeric IgA, and FCRL5, which binds to IgG, may have a role in disease pathology and prognosis. These proteins and their transcripts are often enriched in blood and/or affected tissue of patients with a systemic or organ-specific autoimmune disease like rheumatoid arthritis, Sjögren's disease, systemic lupus erythematous, Graves' disease or myasthenia gravis. The expression of FCRL4 and FCRL5 appears to be disease- and context-specific, and influenced by the tissue microenvironment. Yet, the functions of FCRL proteins are still incompletely understood, and more mechanistic studies are necessary to unravel the contribution of FCRL4 and FCRL5 to pathogenic B-cell responses occurring in autoimmune diseases.

Structural characterization and antitumor activity via immune modulation of an α-glucan from Grifola frondosa.

Delivery routes and circular mRNA vaccine architecture synergistically shape in vivo immune profiles.

Dietary myo-inositol exerts pleiotropic effects on T cell activation, antioxidant defense and fatty acid metabolism to enhance anti-bacterial immunity in tilapia.

Development of anti-CD4-1/CD8β monoclonal antibodies and spatiotemporal immune profiling of response to live attenuated IHNV in rainbow trout (Oncorhynchus mykiss).

Role of triggering receptor expressed on Myeloid Cells-1 (TREM-1) in the prognostic evaluation in bacterial endophthalmitis.

Perineural invasion: A neuroimmune axis mediating immunotherapy resistance across malignancies.

Epidermodysplasia verruciformis (EV) was described as a congenital skin disease and later as a Mendelian disorder in 1922 and 1946, respectively [1]. For decades, EV was considered a monogenic entity and was also interchangeably referred to as Treeman syndrome (TMS). However, recent advancements in next-generation sequencing (NGS) have revealed that the pathogenesis of EV is distinct from TMS [2]. In fact, a recent study showed that TMS, in some cases, is caused by biallelic loss-of-function CD28 mutations and that TMS warts are driven by α-human papillomavirus (HPV) [2]. Furthermore, at least 21 genes have been implicated in EV pathogenesis. Persistent disseminated flat-like warts in EV patients are derived, for the most part, from weakly virulent, E5- and E8-deficient β-HPVs, which exclusively reside within keratinocytes. However, these β-HPVs, lacking the E5 and E8 genes that are expressed in other genera of more pathogenic HPVs, typically cause only asymptomatic infections in the general population [1]. It is noteworthy that, in addition to β-HPVs, non-β-HPVs (including α- and γ-HPVs) are occasionally associated with the EV phenotype [3]. Mechanistic insights gained from studies of single-gene disorders with EV manifestations suggest dual contributions of keratinocyte-intrinsic immunity and adaptive T-cell immunity to β-HPV clearance. Ultrarare and private mutations in genes governing either keratinocyte-intrinsic immunity or adaptive T-cell immunity, at the priming or effector level, confer predisposition to severe β-HPV infections (Figure 1). These observations led Shen et al., in this issue of the International Journal of Dermatology, and other research groups to categorize EV into classic (TMC6, TMC8, and CIB1), nonclassic (e.g., DOCK8, STK4), and acquired forms [4, 5]. A total of 439 EV patients, comprising 137 classic (typical) EV patients, 46 nonclassic (atypical) EV patients, and 256 acquired EV (AEV) patients, were reviewed. The most commonly reported genes were TMC6, CIB1, TMC8, STK4, and DOCK8. A total of 31 distinct HPVs, belonging to the α-, γ-, and β-HPV genera, were associated with the EV phenotype, with β-HPV-5, -8, and -20 identified as the most common types. Collectively, these genomics-driven advances in EV understanding herald a paradigm shift in the diagnosis, prognosis, and monitoring of EV in the era of precision dermatology. While single-gene EV is a pediatric clinical condition (with an age of onset before 12 years in 89% of cases), most AEV patients are adults, and the disease is prevalent among HIV and transplant populations [5]. The phenocopy in AEV patients underscores the effective suppression of the same surveillance pathways for HPV clearance that are disrupted in hereditary forms [4, 5]. A review of oncologic data in EV patients offers clinically actionable insight into the age of onset and extent of cancer risk. The majority (56%) of monogenic EV patients develop malignancy, occurring decades earlier than in the general population. Moreover, the distinction between isolated and syndromic EV has implications for cancer management: cutaneous malignancies predominate in isolated EV, while extracutaneous malignancies are more common in syndromic forms. These results support genotype-informed cancer surveillance strategies in EV patients. Furthermore, they indicate that EV should be integrated into broader hereditary cancer predisposition frameworks [5]. In sum, EV offers a unique human knockout model for the study of host–virus co-evolution, tissue-specific immunity, and early carcinogenesis. Furthermore, recent genomic advances shift the paradigm of EV from a mere dermatologic curiosity to a prototype for precision dermatology. The authors employed large language models to refine manuscript grammar and phrasing, then reviewed, edited, and accepted full responsibility for the final content. The LEO Foundation (grant LF-OC-22-000965) and the US NIH (grant R01AI143810) supported the authors' studies. The authors declare no conflicts of interest. Clinical and Molecular Perspectives on Epidermodysplasia Verruciformis, https://doi.org/10.1111/ijd.70295. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

Activating NK cell immunity against prostate cancer with Hedysarum polybotrys Hand.-Mazz.: A multi-omics integration of computational prediction and experimental validation on PI3K/AKT and PD-1/PD-L1 axes.

ADP-ribosylation is an essential post-translational modification that contributes to key cellular processes, such as DNA damage repair, cell-cycle progression, chromatin remodeling, mitochondrial function, and immune responses in mammalian cells. This modification derives from NAD+ and is regulated by dedicated writer, eraser, and reader proteins that govern its installation, removal, and recognition. Traditionally viewed as a protein-centered modification, ADP-ribosylation has recently been extended to nucleic acids, with ADP-ribosylated DNA and RNA now identified in both mammalian and bacterial systems. These discoveries reveal previously underappreciated layers of nucleic acid-based regulation and suggest that NAD+-dependent chemistry integrates genome maintenance, RNA metabolism, and cellular stress responses. In this review, we first outline the major mammalian ADP-ribosylation machineries, including the families of writer, eraser, and reader proteins, and discuss how their activities are coordinated. We then examine emerging roles of ADP-ribosylation in mitochondria, with a focus on mitochondrial DNA repair and metabolic control. Finally, we highlight recent advances in understanding NAD+-dependent modifications of DNA and RNA in mammalian and bacterial cells, including terminal and nucleobase-linked ADP-ribosylation and NAD capping, and discuss outstanding questions regarding their physiological functions and interplay with protein post-translational modification and other nucleic acid modifications.