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Anti-synthetase syndrome (ASS) is a rare autoimmune myopathy, frequently associated with interstitial lung disease, and is characterized by the presence of anti-aminoacyl tRNA synthetase (ARS) antibodies. However, there have been limited reports of cases exhibiting positive anti-Ha antibodies. This study presents a retrospective analysis of the clinical data from a patient with an acute exacerbation of ASS who tested positive for anti-Ha antibodies. This patient initially presented with interstitial pneumonia. The initial anti-infective treatment was ineffective; however, symptoms improved following the addition of corticosteroids. Upon discontinuation of corticosteroids, the patient experienced a recurrence of cough, progressive worsening of dyspnea, and developed lower general weakness. Comprehensive autoantibody testing revealed positivity for anti-Ha antibodies, and MRI of the lower limbs indicated soft tissue edema. The patient was ultimately diagnosed with ASS with interstitial lung disease. Treatment with methylprednisolone pulse therapy, combined with cyclophosphamide, tacrolimus, tofacitinib citrate, and pirfenidone, led to an improvement in the patient's condition, resulting in discharge. Post-discharge, the patient was maintained on regular oral prednisone, nintedanib, and tofacitinib. Follow-up to date has shown a stable condition, with resolution of pulmonary lesions observed upon re-examination. Anti-Ha antibody is one of the specific antibodies associated with ASS, yet its positive rate remains exceedingly low. This case represents the first reported instance of an anti-Ha antibody-positive ASS in China. Misdiagnosis and missed diagnosis are prevalent in clinical practice, underscoring the importance of screening for autoantibodies when patients present with acute, unexplained interstitial lung changes and a poor response to anti-infective treatment. Furthermore, interstitial lung disease is the most common extra-muscular clinical manifestation observed in ASS patients. Differentiating between acute exacerbations of pulmonary infections and interstitial lung disease associated with rheumatic diseases poses a significant challenge, as both can occur concurrently. Therefore, during diagnosis and treatment, it is crucial to consider not only infections but also to identify the underlying causes of worsening lung lesions.

[This corrects the article DOI: 10.3389/fimmu.2025.1614777.].

Background The airway lesions in COPD are mediated by a variety of inflammatory cells, among which the Th1-dominated delayed-type hypersensitivity response can also cause irreversible damage to normal airways. The immune checkpoint TIGIT and its downstream phosphatase SHIP-1 play a crucial role in coordinating the immune response of CD4 + T cells by regulating the phosphoinositide pathway. Methods This study evaluates the expression patterns of TIGIT/SHIP-1 in CD4 + T cells within the context of smoking-induced COPD and investigates the mechanisms by which TIGIT/SHIP-1 affects CD4 + T cells, also the downstream signaling changes regulating Th1 inflammation. In smoking COPD, we established a research framework encompassing clinical, animal, cellular levels including flow cytometry, immunofluorescence, and chromatin immunoprecipitation. Results We found that CD4 + T cells in smoking COPD exhibit upregulated expression of TIGIT/SHIP-1, and specific knockout of CD4- Tigit and short-term in vivo inhibition of SHIP-1 significantly elevated Th1 levels in emphysematous mice. Through single-cell and bulk-RNA bioinformatics analysis, we identified RelB that regulates COPD-Th1 inflammation by regulates TBX21 in transcriptional level and confirmed its excessive activation in COPD-Th1 inflammation. The PI3K/AKT signaling, acting downstream of TIGIT/SHIP-1, influences the activation of RelB in Th1 cells. Conclusions In smoking-induced COPD, TIGIT/SHIP-1 affects the activation of RelB through the PI3K/AKT pathway, thereby regulating the expression of Th1. It offers insights underlying the immune mechanism of COPD.

Background Semen quality significantly influences conception, and its preservation is crucial for couples seeking pregnancy. We investigated dietary and lifestyle risk factors impacting semen quality. Methods A total of 466 males from the Guangzhou Women and Children’s Medical Center’s pre-pregnancy consultation clinic were recruited between January 2021 and March 2023 for inclusion. Semen analysis was performed, and diet and lifestyle data were gathered via questionnaire. Logistic regression was utilized to examine the link between diet, lifestyle variables, and semen quality. Results Smoking worsened progressive sperm motility (38.0% vs. 36.0%, t = 2.262; P = 0.049). Alcohol consumption impaired progressive motility (40.5 ± 17.8% vs. 34.7 ± 16.1%, t = 3.396; P < 0.001) and total motility (56.0% vs. 64.0%; P = 0.001). Using plastic beverage bottles for oil or seasonings lowered sperm concentrations (40.4% vs. 59.0% vs. 65.5%; P = 0.032). A sweet diet correlated with higher total sperm motility (55.0% vs. 60.0%, 62.0% vs. 63.2%; P = 0.017). Higher milk product intake improved sperm concentration (41.6 10 6 vs. 63.7 10 6 vs. 66.1*10 6 ; P = 0.021) and motility (54.5% vs. 56.0% vs. 63.0%; P = 0.033). More frequent egg consumption increased semen volume (3.1 mL vs. 3.8 mL vs. 4.0 mL; P = 0.038). Roughage intake enhanced sperm concentration (160.8 10 6 vs. 224.6 10 6 ; P = 0.027), and adequate sleep improved progressive sperm motility rate (35.4% ± 18.2% vs. 40.2 ± 16.3%, F = 3.747; P = 0.024) and total motility (52.7% vs. 61.5%; P = 0.013). The regression model showed that using plastic containers for condiments was a protective factor for semen volume (OR: 0.12; CI 0.03–0.55; P = 0.006), sperm concentration (OR: 0.001, CI 0.00–0.30; P = 0.012), and count (OR: 0.12, CI 0.03–0.48; P = 0.003). Milk and egg consumption were also protective for semen volume (OR: 0.18, CI 0.06–0.51; P = 0.001 and OR: 0.11, CI 0.03–0.55; P = 0.006, respectively), while sufficient sleep benefitted total sperm motility (OR: 0.47, CI 0.24–0.95; P = 0.034). Conclusions Smoking and drinking, type of condiment container, diet preference, sleep duration, and milk, roughage, and egg consumption may reduce semen quality.

IFN-γ+CD4+ cells (type 1 helper T cells, Th1) represent a critical component of the inflammatory environment in the lungs of chronic obstructive pulmonary disease (COPD). Identifying influencing factors related to COPD-associated Th1 cells will enhance our understanding of the inflammatory mechanisms involved and facilitate the development of targeted interventions. We describe T-cell immunoglobulin and mucin-domain containing-3 (Tim3) as a key gene regulating COPD-associated Th1 cells through single-cell sequencing, flow cytometry and knockout mice. Our findings indicate that Havcr2 expression gradually increases during CD4+ T cell activation in COPD mice, with Tim3 being highly expressed on both CD4+ T cells and Th1 cells. Notably, the knockout of HAVCR2 further promotes the infiltration of CD4+ T cells and the expression of IFN-γ in the lungs, resulting in a more severe emphysema phenotype, although it does not significantly affect TNF-α expression. Additionally, NFIL3, an upstream regulator of Tim3, is also highly expressed in the CD4+ T cells of COPD mice. Mice with NFIL3 knockout exhibit phenotypes similar to those of HAVCR2 knockout mice, along with a significant downregulation of Tim3 expression. , we simulated the activation process by polarizing primary CD4+ Tn cells from COPD mice and observed that NFIL3/Tim3 expression was significantly upregulated following Th1 polarization. Our study demonstrates that the NFIL3/Tim3 axis plays a role in Th1 imbalance in the lungs of COPD by inhibiting Th1 differentiation.

Sperm quality can be easily influenced by living environmental and occupational factors. This study aimed to discover potential semen quality related living environmental and occupational factors, expand knowledge of risk factors for semen quality, strengthen men's awareness of protecting their own fertility and assist the clinicians to judge the patient’s fertility. 465 men without obese or underweight (18.5 < BMI < 28.5 kg/m 2 ), long-term medical history and history of drug use, were recruited between June 2020 to July 2021, they are in reproductive age (25 < age < 45 years). We have collected their semen analysis results and clinical information. Logistic regression was applied to evaluate the association of semen quality with different factors. We found that living environment close to high voltage line (283.4 × 10 6 /ml vs 219.8 × 10 6 /ml, Cohen d  = 0.116, P = 0.030) and substation (309.1 × 10 6 /ml vs 222.4 × 10 6 /ml, Cohen d  = 0.085, P = 0.015) will influence sperm count. Experienced decoration in the past 6 months was a significant factor to sperm count (194.2 × 10 6 /ml vs 261.0 × 10 6 /ml, Cohen d  = 0.120, P = 0.025). Living close to chemical plant will affect semen PH (7.5 vs 7.2, Cohen d  = 0.181, P = 0.001). Domicile close to a power distribution room will affect progressive sperm motility (37.0% vs 34.0%, F = 4.773, Cohen d  = 0.033, P = 0.030). Using computers will affect both progressive motility sperm (36.0% vs 28.1%, t = 2.762, Cohen d  = 0.033, P = 0.006) and sperm total motility (57.0% vs 41.0%, Cohen d  = 0.178, P = 0.009). After adjust for potential confounding factors (age and BMI), our regression model reveals that living close to high voltage line is a risk factor for sperm concentration (Adjusted OR 4.03, 95% CI 1.15–14.18, R 2  = 0.048, P = 0.030), living close to Chemical plants is a protective factor for sperm concentration (Adjusted OR 0.15, 95% CI 0.05–0.46, R 2  = 0.048, P = 0.001) and total sperm count (Adjusted OR 0.36, 95% CI 0.13–0.99, R 2  = 0.026, P = 0.049). Time spends on computer will affect sperm total motility (Adjusted OR 2.29, 95% CI 1.11–4.73, R 2  = 0.041, P = 0.025). Sum up, our results suggested that computer using, living and working surroundings (voltage line, substation and chemical plants, transformer room), and housing decoration may association with low semen quality. Suggesting that some easily ignored factors may affect male reproductive ability. Couples trying to become pregnant should try to avoid exposure to associated risk factors. The specific mechanism of risk factors affecting male reproductive ability remains to be elucidated.

Background: LncRNAs play diverse roles and participate in various biological processes within the human body. It has been frequently reported that they are involved in the occurrence and development of recurrent spontaneous miscarriage. PRNCR1, a crucial player in several types of cancers, may also have implications for recurrent spontaneous miscarriage risk. However, the correlation between PRNCR1 rs13252298 A > G polymorphism and this risk remains unclear. In summary, we conducted the following experiments to investigate the association between the PRNCR1 polymorphic site rs13252298 and susceptibility to recurrent spontaneous miscarriage. Method: Our research included 695 healthy controls and 413 patients with recurrent spontaneous miscarriage from southern China. Genotyping was performed using the TaqMan method. Result: Our findings revealed that there is a relationship between PRNCR1 rs13252298 A > G polymorphism and lower susceptibility to recurrent spontaneous miscarriage (AG and AA: adjusted OR = 0.794, 95% CI = 0.527–1.196, p = 0.2696; GG and AA: adjusted OR = 0.705, 95% CI = 0.542–0.917, p = 0.0092; dominant model: adjusted OR = 0.722, 95% CI = 0.563–0.926, p = 0.0104; recessive model: adjusted OR = 0.949, 95% CI = 0.644–1.398, p = 0.7912). Conclusion: The results of our study demonstrate that the PRNCR1 rs13252298 A > G allele may contribute to a decreased risk of recurrent spontaneous miscarriage. The rs13252298 polymorphism could potentially serve as a biomarker for detecting recurrent spontaneous miscarriage risk and aiding prevention efforts.

TIGIT, a co-inhibitory receptor found on T cells and NK cells, transmits inhibitory signals upon binding to its ligand. This interaction suppresses the activation of various signaling pathways, leading to functional exhaustion of cells, ultimately dampening excessive inflammatory responses or facilitating immune evasion in tumors. Dysregulated TIGIT expression has been noted in T cells across different inflammatory conditions, exhibiting varying effects based on T cell subsets. TIGIT predominantly restrains the effector function of pro-inflammatory T cells, upholds the suppressive function of regulatory T cells, and influences Tfh maturation. Mechanistically, the IL27-induced transcription factors c-Maf and Blimp-1 are believed to be key regulators of TIGIT expression in T cells. Notably, TIGIT expression in T cells is implicated in lung diseases, particularly airway inflammatory conditions such as lung cancer, obstructive pulmonary disease, interstitial lung disease, sarcoidosis, and COVID-19. This review emphasizes the significance of TIGIT in the context of T cell immunity and airway inflammatory diseases.

Asynchronous wake-up communication based on wake-up radio (WuR) is an important energy-saving method in wireless sensor networks (WSNs). The Clear Channel Assessment (CCA) is a major section of energy consumption in asynchronous WuR-based nodes. The traditional static backoff will lead to longer waiting delay which increase the energy consumption of successful sending packets when the network traffic becomes heavier. So a protocol DNAP-WuR is proposed to solve these problems in the terminal initiated (TI) communication mode. It first implements the dynamic CCA optimization (DCO) mechanism which allows nodes to interrupt the CCA process as soon as the channel is busy. Nodes can go to sleep faster during busy periods, instead of performing CCA detection until the counter is reduced to zero. And then, the WuR based adaptive logarithm backoff (WALB) algorithm is used to predict the backoff time sequences which can reduce the WuC's collision probability and decrease the energy consumption according to the nodes number and the packet arrival rate. In order to avoid the phenomenon that the backoff window size is reduced too fast or increased slowly after packets transmitted. Compared with CSMA-WuR protocol, the DNAP-WuR has 4.6% reduction in energy consumption and 12.1% promotion in throughput.

Background: Nano-selenium has been widely used in antiviral and anticancer therapy, and has the advantages of good targeting and low toxicity. For the first time, we combined male reproduction with nano-selenium to investigate its antioxidant effect. This study investigated the protective effect of lentinan functionalized selenium nanoparticles on oxidative stress injury of the hydrogen peroxide (H2O2)-induced Leydig cell line, TM3. Methods: The suitable concentration of nano-selenium treatment to promote cell proliferation was also discussed. The concentration of 4 μM could significantly promote the growth of TM3 cells. Oxidative stress damage was caused using an 800 μM concentration of hydrogen peroxide. The cells were divided into four groups: normal control group, oxidative stress treatment group, H2O2+SeNPs@LNT group, and SeNPs@LNT group. The H2O2+SeNPs@LNT group was pretreated with 4 μM of SeNPs@LNT for 12 h, followed by 800 μM of H2O2 for 8 h. Results: Nano-selenium could significantly promote the proliferation and viability of TM3 cells. SeNPs@LNT treatment increased the level of mitochondrial membrane potential in normal cells and slowed down the decline in mitochondrial membrane potential level caused by oxidative stress injury. In addition, the increase in reactive oxygen species caused by oxidative stress was inhibited by SeNPs@LNT treatment. The apoptosis of TM3 cells was detected, and SeNPs@LNT alleviated the necrosis and apoptosis of TM3 cells induced by H2O2. Nano-selenium plays a protective role against oxidative H2O2-induced stress injury in TM3 cells through the changes in the Janus kinase 2/signal transducer and activator of transcription 3 signaling pathway and P53 pathway, and the expression levels of other related proteins, protein kinase B (AKT) and C3. Conclusion: SeNPs@LNT exhibited good biological activity and antioxidant effect and can thus be used to protect the male reproductive system from oxidative stress.