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Background The transplantation of exosomes derived from human adipose-derived mesenchymal stem cells (hADSCs) has emerged as a prospective cellular-free therapeutic intervention for the treatment of neurodevelopmental disorders (NDDs), as well as autism spectrum disorder (ASD). Nevertheless, the efficacy of hADSC exosome transplantation for ASD treatment remains to be verified, and the underlying mechanism of action remains unclear. Results The exosomal long non-coding RNAs (lncRNAs) from hADSC and human umbilical cord mesenchymal stem cells (hUCMSC) were sequenced and 13,915 and 729 lncRNAs were obtained, respectively. The lncRNAs present in hADSC-Exos encompass those found in hUCMSC-Exos and are associated with neurogenesis. The biodistribution of hADSC-Exos in mouse brain ventricles and organoids was tracked, and the cellular uptake of hADSC-Exos was evaluated both in vivo and in vitro. hADSC-Exos promote neurogenesis in brain organoid and ameliorate social deficits in ASD mouse model BTBR T + tf/J (BTBR). Fluorescence in situ hybridization (FISH) confirmed lncRNA Ifngas1 significantly increased in the prefrontal cortex (PFC) of adult mice after hADSC-Exos intraventricular injection. The lncRNA Ifngas1 can act as a molecular sponge for miR-21a-3p to play a regulatory role and promote neurogenesis through the miR-21a-3p/PI3K/AKT axis. Conclusion We demonstrated hADSC-Exos have the ability to confer neuroprotection through functional restoration, attenuation of neuroinflammation, inhibition of neuronal apoptosis, and promotion of neurogenesis both in vitro and in vivo. The hADSC-Exos-derived lncRNA IFNG-AS1 acts as a molecular sponge and facilitates neurogenesis via the miR-21a-3p/PI3K/AKT signaling pathway, thereby exerting a regulatory effect. Our findings suggest a potential therapeutic avenue for individuals with ASD. Graphical Abstract

Brucellosis is the most common bacterial zoonotic infection. This pathogen may survive and sustain in host. The aim of this study is to define relationship between long noncoding (lnc) RNA-IFNG-AS1 and interferon gamma (IFN-γ) in different groups of patients with brucellosis compared to control group. In this study, associations of lncRNA IFNG-AS1 expression with secretion of IFN-γ level in Sixty patients with brucellosis, which were divided into 3 groups (acute, chronic and relapse groups), as a case group were compared with 20 subjects with negative serological tests and brucellosis clinical manifestation as a control group. In this regard, RNA were extracted from isolated peripheral blood mononuclear cells (PBMCs). LncRNA IFNG-AS1, T-box transcription factor (T-bet) and IFN-γ expressions were detected using quantitative polymerase chain reaction (qPCR). Serum level IFN-γ was assessed using enzyme linked immunosorbent assay (ELISA). The results showed that expression level of LncRNA IFNG-AS1, T-bet and IFN-γ increased significantly in all patient groups in compared to healthy subjects (P < 0.0001, P < 0.01, P < 0.001). However, there was no significant difference in T-bet expression between chronic and healthy groups (P = 0.98). Additionally, further analysis revealed that the serum level of IFN-γ in acute and relapsed groups were higher than control group (P < 0.0001, P < 0.001). The effective role of IFNG-AS1 in many protective actions, including enhancing the expression of INF-γ in the immune response of brucellosis patients, revealed new potential marker, LncRNA IFNG-AS1 in screening, diagnosis or treatment of brucellosis.

Recent studies have shown dysregulation of several groups of long non-coding RNAs in the context of epilepsy. According to evidence regarding the role of regulatory T cells in this disorder, we examined expression levels of regulatory T cell-related lncRNAs, namely TH2-LCR, RMRP, IFNG-AS1 (NEST), MAFTRR and FLICR in the blood of epileptic cases compared with controls. Expression of RMRP was lower in patients with refractory epilepsy compared with controls [expression ratio (95% CI) = 0.32 (0.13–0.8), adjusted p -value = 0.0008]. Besides, its expression was lower in refractory patients vs. non-refractory patients [expression ratio (95% CI) = 0.2 (0.1–0.41), adjusted p -value < 0.0001]. Expression of TH2-LCR was lower in refractory patients vs. controls [expression ratio (95% CI) = 0.4 (0.17–0.93), adjusted p -value = 0.0044] and in refractory patients vs. non-refractory ones [Expression ratio = 0.28 (0.19–0.58), p -value < 0.0001]. Expression of NEST was higher in total patients [expression ratio (95% CI) = 2.48 (1.15–5.27), adjusted p -value = 0.0012] and in both groups of patients compared with controls. However, its expression was not different between refractory and non-refractory cases. Similarly, FLICR and MAFTRR were over-expressed in total cases and both groups of patients compared with controls, but their expressions were similar between refractory and non-refractory cases. MAFTRR could differentiate between total epileptic cases and controls with AUC value of 0.8. This lncRNA could separate refractory and non-refractory cases from healthy controls with AUC values of 0.73 and 0.88, respectively. This study provides evidence for deregulation of regulatory T cell-related lncRNAs in epilepsy and their potential role as diagnostic markers in this condition.

The prevalence of autoimmune diseases ranks as the third most common disease category globally, following cancer and heart disease. Numerous studies indicate that long non-coding RNA (lncRNA) plays a pivotal role in regulating human growth, development, and the pathogenesis of various diseases. It is more than 200 nucleotides in length and is mostly involve in the regulation of gene expression. Furthermore, lncRNAs are crucial in the development and activation of immune cells, with an expanding body of research exploring their association with autoimmune disorders in humans. LncRNA Ifng antisense RNA 1 (IFNG-AS1), a key regulatory factor in the immune system, also named NeST or TMEVPG1, is proximally located to IFNG and participates in the regulation of it. The dysregulation of IFNG-AS1 is implicated in the pathogenesis of several autoimmune diseases. This study examines the role and mechanism of IFNG-AS1 in various autoimmune diseases and considers its potential as a therapeutic target.

Background Lung cancer is the second most prevalent malignancy among males and females and the leading cause of cancer deaths. Due to its high mortality, identification of novel therapeutic options is of critical value. Regulatory T cells and their associated transcripts are among possible targets for design of targeted therapies. Methods Here, we assessed expression of lncRNAs that are possibly involved in Treg lineage commitment and their plasticity in lung tumor tissues (TT) and normal tissues adjacent to the tumor (NTAT). Results We found up-regulation of TH2-LCR, IFNG-AS1, and MAFTRR in TT samples compared with NTATs. The highest difference in the expression between two sets of samples belonged to MAFTRR with expression ratio (95% CI) of 6.48 (2.67–15.7). TH2-LCR ranked second in this list with expression ratio (95% CI) of 5.23 (1.92–14.24). Finally, IFNG-AS1 was up-regulated in TT samples compared with NTATs with expression ratio (95% CI) of 3.3 (1.56–6.95). Then, the suitability of MAFTRR, TH2-LCR and IFNG-AS1 in the separation of TT samples from NTATs was assessed through plotting sensitivity values against 1-specifiicity values in ROC curves. The obtained AUC values were 0.74, 0.71 and 0.7, respectively. Conclusion In brief, we demonstrated dysregulation of three Treg-related lncRNAs in lung cancer tissues and suggested them as possible candidates for biomarker discovery investigations.