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microti infection. The concentrations of hemoglobin in rBmSP44 immunization group were higher than those in the control group. Importantly, vaccination of mice with rBmSP44 resulted in a Th1/Th2 mixed immune response with significantly elevated IL-10 and IFN-γ levels during the early stage of infection. Taken together, our results indicated that rBmSP44 can induce a protective immune response against Babesia infection. Thus, BmSP44 can be used as both a diagnosis marker and a vaccine candidate.Therapeutic corticosteroids have an immunosuppressive function involving several pathways, including lymphocytopenia and hypogammaglobulinemia. While these effects have been well-described in patients that received corticosteroids for therapeutic reasons, the effects of endogenous corticosteroids on the immune system are less well-understood. NSC 663284 Here, we describe a 21-year old patient with hypercortisolism due to an ACTH producing thymic tumor. In this patient, we observed a decrease in some of the immunoglobulin classes, and in specific B and T cell populations that resembled effects caused by corticosteroid treatment. IgG levels were restored following treatment and normalization of the hypercortisolism.The innate immune response to cytosolic DNA involves transcriptional activation of type I interferons (IFN-I) and proinflammatory cytokines. This represents the culmination of intracellular signaling pathways that are initiated by pattern recognition receptors that engage DNA and require the adaptor protein Stimulator of Interferon Genes (STING). These responses lead to the generation of cellular and tissue states that impair microbial replication and facilitate the establishment of long-lived, antigen-specific adaptive immunity. Ultimately this can lead to immune-mediated protection from infection but also to the cytotoxic T cell-mediated clearance of tumor cells. Intriguingly, pharmacologic activation of STING-dependent phenotypes is known to enhance both vaccine-associated immunogenicity and immune-based anti-tumor therapies. Unfortunately, the STING protein exists as multiple variant forms in the human population that exhibit differences in their reactivity to chemical stimuli and in the intensity of molecular signaling they induce. In light of this, STING-targeting drug discovery efforts require an accounting of protein variant-specific activity. Herein we describe a small molecule termed M04 that behaves as a novel agonist of human STING. Importantly, we find that the molecule exhibits a differential ability to activate STING based on the allelic variant examined. Furthermore, while M04 is inactive in mice, expression of human STING in mouse cells rescues reactivity to the compound. Using primary human cells in ex vivo assays we were also able to show that M04 is capable of simulating innate responses important for adaptive immune activation such as cytokine secretion, dendritic cell maturation, and T cell cross-priming. Collectively, this work demonstrates the conceivable utility of a novel agonist of human STING both as a research tool for exploring STING biology and as an immune potentiating molecule.The present study investigated the transcriptomic response of porcine dendritic cells (DC) to innate stimulation in vitro and in vivo. The aim was to identify DC subset-specialization, suitable Toll-like receptor (TLR) ligands targeting plasmacytoid DC (pDC), and the DC activation profile during highly and low virulent classical swine fever virus (CSFV, strain Eystrup and Pinar del Rio, respectively) infection, chosen as model for a virus causing a severe immunopathology. After identification of porcine conventional DC (cDC) 1, cDC2, pDC and a monocyte-derived subset in lymphoid tissues, we characterized DC activation using transcriptomics, and focused on chemokines, interferons, cytokines, as well as on co-stimulatory and inhibitory molecules. We demonstrate that porcine pDC provide important signals for Th1 and interferon responses, with CpG triggering the strongest responses in pDC. DC isolated early after infection of pigs with either of the two CSFV strains showed prominent upregulation of CCL5, CXCL9, CXCL10, CXCL11, and XCL1, as well as of the cytokines TNFSF13B, IL6, IL7, IL12B, IL15, IL27. Transcription of IL12B and many interferon genes were mostly restricted to pDC. Interestingly, the infection was associated with a prominent induction of inhibitory and cell death receptors. When comparing low and highly virulent CSFV strains, the latter induced a stronger inflammatory and antiviral response but a weaker cell cycle response, and reduced antigen presentation functions of DC. Taken together, we provide high-resolution information on DC activation in pigs, as well as information on how DC modulation could be linked to CSFV immunopathology.Success in cancer treatment over the last four decades has ranged from improvements in classical drug therapy to immune oncology. Anti-cancer drugs have also often proven beneficial for the treatment of inflammatory and autoimmune diseases. In this review, we report on challenging examples that bridge between treatment of cancer and immune-mediated diseases, addressing mechanisms and experimental models as well as clinical investigations. Patient-derived tumor xenograft (PDX) (humanized) mouse models represent useful tools for preclinical evaluation of new therapies and biomarker identification. However, new developments using human ex vivo approaches modeling cancer, for example in microfluidic human organs-on-chips, promise to identify key molecular, cellular and immunological features of human cancer progression in a fully human setting. Classical drugs which bridge the gap, for instance, include cytotoxic drugs, proteasome inhibitors, PI3K/mTOR inhibitors and metabolic inhibitors. Biologicals developed for cancer therapy have also shown efficacy in the treatment of autoimmune diseases. In immune oncology, redirected chimeric antigen receptor (CAR) T cells have achieved spectacular remissions in refractory B cell leukemia and lymphoma and are currently under development for tolerance induction using cell-based therapies such as CAR Tregs or NK cells. Finally, a brief outline will be given of the lessons learned from bridging cancer and autoimmune diseases as well as tolerance induction.