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5%. Our findings in S. viridis suggest that manipulation of Atcel1 has potential for developing early-maturing and higher-yielding monocotyledonous biomass crops suitable for climate-smart agriculture.Oxidized cholesterols have emerged as important signaling molecules of immune function, but little is known about the role of these oxysterols during mycobacterial infections. We found that expression of the oxysterol-receptor GPR183 was reduced in blood from patients with tuberculosis (TB) and type 2 diabetes (T2D) compared to TB patients without T2D and was associated with TB disease severity on chest x-ray. GPR183 activation by 7α,25-dihydroxycholesterol (7α,25-OHC) reduced growth of Mycobacterium tuberculosis (Mtb) and Mycobacterium bovis BCG in primary human monocytes, an effect abrogated by the GPR183 antagonist GSK682753. Growth inhibition was associated with reduced IFN-β and IL-10 expression and enhanced autophagy. Mice lacking GPR183 had significantly increased lung Mtb burden and dysregulated IFNs during early infection. Together, our data demonstrate that GPR183 is an important regulator of intracellular mycobacterial growth and interferons during mycobacterial infection.CD4+Foxp3+Tregs maintain immune homeostasis, but distinct mechanisms underlying their functional heterogeneity during infections are driven by specific cytokine milieu. Here we show that MyD88 deletion in Foxp3+ cells altered their function and resulted in increased fungal burden and immunopathology during oral Candida albicans (CA) challenge. Excessive inflammation due to the absence of MyD88 in Tregs coincided with a reduction of the unique population of IL-17A expressing Foxp3+ cells (Treg17) and an increase in dysfunctional IFN-γ+/Foxp3+ cells (TregIFN-γ) in infected mice. Failure of MyD88-/- Tregs to regulate effector CD4+ T cell functions correlated with heightened levels of IFN-γ in CD4+ T cells, as well as increased infiltration of inflammatory monocytes and neutrophils in oral mucosa in vivo. Mechanistically, IL-1β/MyD88 signaling was required for the activation of IRAK-4, Akt, and mTOR, which led to the induction and proliferation of Treg17 cells. In the absence of IL-1 receptor signaling, Treg17 cells were reduced, but IL-6-driven expansion of TregIFN-γ cells was increased. This mechanism was physiologically relevant during Candida infection in aged mice, as they exhibited IL-1 receptor/MyD88 defect in Foxp3+ cells, loss of p-mTORhighTreg17 cells and reduced levels of IL-1β in oral mucosa, which coincided with persistent tongue inflammation. Concurrent with Treg dysfunction, aging was associated with increased CD4+ T cell hyperactivation and heightened levels of IL-6 in mice and humans in oral mucosa in vivo. Taken together, our data identify IL-1β/MyD88/Treg axis as a new component that modulates inflammatory responses in oral mucosa. Also, dysregulation of this axis in an aging immune system may skew host defense towards an immunopathological response in mucosal compartments.Recently, the immuno-enhancing potential of polysaccharide from Auricularia auricula (AAP) has been an area of research interest. However, the immune-stimulatory activity and mechanisms of AAP in immunosuppressive mice treated with cyclophosphamide (CTX) are still poorly understood. This study aimed to evaluate the immuno-enhancing effects of AAP and mine its possible mechanisms. Firstly, polysaccharides were isolated from A. auricula and purified. Secondly, the immune-stimulatory activities of the first AAP fraction (AAP1) were evaluated in the CTX-treated mice. Results showed that AAP1 significantly enhanced immune organ indexes, remarkably stimulated IFN-γ, IL-2, IL-4, IL-10, and TNF-α levels in the serum, and dramatically up-regulated the mRNA levels of Claudin-1, Occludin and ZO-1. Compared to the CTX group, AAP1 administration restored the gut microbiota composition similar to that of the control group by decreasing the ratio of Firmicutes/Bacteroidetes and increasing the relative abundances of short-chain fatty acid-producing microbiota. This study provides useful information for its further application as an immune-stimulator in foods and drugs.Trypanosoma cruzi and Toxoplasma gondii are two parasites than can be transmitted from mother to child through the placenta. However, congenital transmission rates are low for T. cruzi and high for T. gondii. Infection success or failure depends on complex parasite-host interactions in which parasites can alter host gene expression by modulating non-coding RNAs such as miRNAs. [https://www.selleckchem.com/products/glutathione.html GSH purchase] As of yet, there are no reports on altered miRNA expression in placental tissue in response to either parasite. Therefore, we infected human placental explants ex vivo by cultivation with either T. cruzi or T. gondii for 2 h. We then analyzed the miRNA expression profiles of both types of infected tissue by miRNA sequencing and quantitative PCR, sequence-based miRNA target prediction, pathway functional enrichment, and upstream regulator analysis of differentially expressed genes targeted by differentially expressed miRNAs. Both parasites induced specific miRNA profiles. GO analysis revealed that the in silico predicted targets of the differentially expressed miRNAs regulated different cellular processes involved in development and immunity, and most of the identified KEGG pathways were related to chronic diseases and infection. Considering that the differentially expressed miRNAs identified here modulated crucial host cellular targets that participate in determining the success of infection, these miRNAs might explain the differing congenital transmission rates between the two parasites. Molecules of the different pathways that are regulated by miRNAs and modulated during infection, as well as the miRNAs themselves, may be potential targets for the therapeutic control of either congenital Chagas disease or toxoplasmosis.Immune checkpoint inhibitors (ICIs) have ushered in a new era of cancer therapy; however, ICIs are only effective in selective patients. The efficacy of ICIs is closely related to the tumor microenvironment. Fever for a long time was thought to directly regulate the immune response, and artificial "fever" from hyperthermia modulates the tumor immune microenvironment by providing danger signals with heat shock proteins (HSPs) as well as subsequent activation of immune systems. Encouraging results have been achieved in preclinical studies focused on potential synergetic effects by combining hyperthermia with ICIs. In this review, we summarized a cluster of immune-related factors that not only make hyperthermia a treatment capable of defending against cancer but also make hyperthermia a reliable treatment that creates a type I-like tumor microenvironment (overexpression of PD-L1 and enrichment of tumor infiltrating lymphocytes) in complementary for the enhancement of the ICIs. Then we reviewed recent preclinical data of the combination regimens involving hyperthermia and ICIs that demonstrated the combined efficacy and illustrated possible approaches to further boost the effectiveness of this combination.