【Objective】 To study the characteristics of HIV infection among voluntary blood donors in Shijiazhuang from 2011 to 2021, so as to provide reference for decision making in the control of HIV for blood centers. 【Methods】 The confirmatory results of HIV reactive samples in initial screening among voluntary blood donors from 2011 to 2021 in our center were statistical analyzed. 【Results】 A total of 2 008 299 samples from 1 667 315 blood donors were detected, among which 3 217 samples were HIV reactive and 234 were confirmed positive, with the positive rate at 11.65/100 000 and the prevalence of 14.03/100 000. The prevalence in men was higher than that in women (16.52/100 000 vs 1.39/100 000), in first-time blood donors higher than that in repeated donors (17.27/100 000 vs 8.12/100 000), in whole blood donors higher than that in plateletpheresis donors (12.01/100 000 vs 8.41/100 000), and the differences were statistically significant (P<0.05). The male homosexual transmission was the main routes of transmission, accounting for 62.39% (146/234). And 72% of double-reagent reactive samples were confirmed positive. Four samples were screened in the serological window period and 6 samples were from HIV positive confirmed donors. 【Conclusion】 The HIV prevalence among voluntary blood donors in Shijiazhuang was low. A certain percentage of repeated blood donors got newly infected. NAT could shorten the detection window period of HIV. Since some confirmed positive samples had not been detected out by NAT, publicity and education should be strengthened to reduce the probability of infected or high-risk groups to participate in blood donation.

Tolerogenic dendritic cells (tolDCs) facilitate the suppression of autoimmune responses by differentiating regulatory T cells (Treg). The dysfunction of immunotolerance results in the development of autoimmune diseases, such as rheumatoid arthritis (RA). As multipotent progenitor cells, mesenchymal stem cells (MSCs), can regulate dendritic cells (DCs) to restore their immunosuppressive function and prevent disease development. However, the underlying mechanisms of MSCs in regulating DCs still need to be better defined. Simultaneously, the delivery system for MSCs also influences their function. Herein, MSCs are encapsulated in alginate hydrogel to improve cell survival and retention in situ, maximizing efficacy in vivo. The three-dimensional co-culture of encapsulated MSCs with DCs demonstrates that MSCs can inhibit the maturation of DCs and the secretion of pro-inflammatory cytokines. In the collagen-induced arthritis (CIA) mice model, alginate hydrogel encapsulated MSCs induce a significantly higher expression of CD39⁺CD73⁺ on MSCs. These enzymes hydrolyze ATP to adenosine and activate A_2A/2B receptors on immature DCs, further promoting the phenotypic transformation of DCs to tolDCs and regulating naïve T cells to Tregs. Therefore, encapsulated MSCs obviously alleviate the inflammatory response and prevent CIA progression. This finding clarifies the mechanism of MSCs-DCs crosstalk in eliciting the immunosuppression effect and provides insights into hydrogel-promoted stem cell therapy for autoimmune diseases.

Monocytes are key effectors in autoimmunity-related diseases in the central nervous system (CNS) due to the critical roles of these cells in the production of proinflammatory cytokines, differentiation of T-helper (Th) cells, and antigen presentation. The JAK-STAT signaling is crucial for initiating monocytes induced immune responses by relaying cytokines signaling. However, the role of this pathway in modulating the communication between monocytes and Th cells in the pathogenesis of multiple sclerosis (MS) is unclear. Here, we show that the JAK1/2/3 and STAT1/3/5/6 subtypes involved in the demyelination mediated by the differentiation of pathological Th1 and Th17 and the CNS-infiltrating inflammatory monocytes in experimental autoimmune encephalomyelitis (EAE), a model for MS. JAK inhibition prevented the CNS-infiltrating CCR2-dependent Ly6C^hi monocytes and monocyte-derived dendritic cells in EAE mice. In parallel, the proportion of GM-CSF⁺CD4⁺ T cells and GM-CSF secretion were decreased in pathological Th17 cells by JAK inhibition, which in turns converted CNS-invading monocytes into antigen-presenting cells to mediate tissue damage. Together, our data highlight the therapeutic potential of JAK inhibition in treating EAE by blocking the GM-CSF-driven inflammatory signature of monocytes.