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The application of platelet-rich plasma (PRP) in wound repair is progressively garnering attention. However, certain patients, owing to relative or absolute contraindications, encounter impediments in the acquisition or application of autologous PRP. The utilization of homologous allogeneic PRP, sourced through rigorous donor selection and standardized preparation methodologies, as a substitute for autologous PRP, may hold favorable implications for such individuals. This article endeavors to succinctly delineate and forecast the mechanisms, advantages, limitations, efficacy and safety of allogeneic PRP in the context of wound healing, furnishing a foundation for its implementation in wound repair.

Objective To investigate the effects of platelet activation pathways on the characterization of platelet-derived extracellular vesicles(PEVs). Methods Whole blood from healthy donors was prepared into platelet suspension by centrifugation. Platelets were randomly divided into six groups, the ctrl group added no extra stimulus, and the other five groups were treated with collagen, adenosine diphosphate(ADP), thrombin, Ca2+ ionophore and freeze-thaw cycles (F-T) to activate platelets. Platelet-derived exosomes(PEXOs) and microvesicles(PMVs) were isolated by differential centrifugations, and then were determined by nano-flow cytometry and electron microscopy. The protein markers of PEXOs also were identified by western-blot. The protein concentration and content of PEXOs were also detected. Results CD9, CD81, TSG101 proteins were detected in all of the PEXOs, which had no calnexin. Both PEXOs and PMVs had CD41; PEXOs were cup-holder-like bilayer membrane vesicles under a transmission electron microscope, while PMVs were irregular membranous structure; 85%-95% of PEXOs were

Activated platelets secrete bioactive molecules and extracellular vesicles. Platelet-derived extracellular vesicles(PEVs), which are rich in proteins, have become important mediators of intercellular communication and cargo exchange, being involved in not only hemostasis and thrombosis, but also in immunity and tissue repair. In past decades, many advances have been made in the isolation, characterization and application of PEVs. Platelet activation modes influence the proteomic features of formed extracellular vesicles. The activation ways may be closely related to functional differences. This review summarized the proteomics and functions of PEVs induced by different platelet activation pathways.

Objective To optimize the preparation conditions of platelets as biomarkers to ensure the preparation of platelet samples with low activation and good stability. Methods The platelet count, platelet activation rate and the count of residual leukocytes were compared among the control and four experimental groups with different centrifugation conditions (120g 10 min vs. 120g 15 min vs.120g 20 min vs.240g 20 min)and different formulations of protective solution, i.e.apyrase, dipyridamole, cilostazol and L-arginine (experimental group 1) vs.apyrase, dipyridamole, cilostazol and adenosine (experimental group 2) vs.apyrase, cilostazol, L-Arginine and adenosine (experimental group 3) vs. apyrase, dipyridamole, L-arginine and adenosine (experimental group 4). Results Platelets obtained by centrifugation at 120 g for 15 min(73.88±5.36) and centrifugation at 120 g for 10 min(77.65±3.07) had higher recovery rates than other experimental groups(52.77±7.86 and 37.71±13.82)(P0.05). The residual leukocytes in the experimental group centrifuged at 120g for 15 min was slightly lower than that in the experimental group centrifuged at 120 g for 10 min, with no statistical differences (P>0.05). The platelet activation rates of four experimental groups were all significantly lower than that of the control within 72 hours (P0.05). Conclusion For preparing platelets as biomarker samples, the group with solution including apyrase, dipyridamole, cilostazol and L-arginine, and centrifugation at 120 g for 15min, showed the minimum residual leukocytes and the optimum stability within 72 hours.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease affecting the colon and rectum, in which the abnormality of B cells is involved in both its pathogenesis and progression. Follicular helper T cells (TFH) play an important role in assisting the immune function of human B cells in germinal centers, and follicular regulatory T cells (TFR) have the function of inhibiting TFH and germinal center B cell responses. The significance of circulating TFH and TFR in ulcerative colitis (UC) remains unclear. We analyzed peripheral blood of active and stable remission UC patients and found that circulating TFR was significantly decreased while TFH was increased in active UC patients. As to TFH subsets, TFH2 was elevated while TFH17 was decreased in active UC, with IL-4/IL-17A secretion enhanced. Helios+ and CD45RA−FoxP3high TFR cells were decreased while CD226+ and CD45RA+FoxP3int TFR cells were increased in active UC patients. The levels of new memory B cells, plasmablasts and serum IgG were significantly increased in active UC patients, and were positively correlated with TFH and TFH2, and negatively correlated with TFR. Serum CRP and Mayo Clinic scores were positively correlated with TFH and TFH2 but negatively correlated with TFR. Serum IL-12 and IL-21 were up-regulated while IL-10 was down-regulated in active UC. To conclude, an imbalance of circulating TFH and TFR cells is associated with disease activity in UC patients. Our results suggest a new mechanism for TFH and TFR imbalance in the pathogenesis of UC, providing a new perspective for theoretical research and therapeutic strategies for UC.

Background. This study is aimed at exploring the changes and significance of circulating Th and Tfh cell subsets in glucocorticoid-treated IgG4-RD patients. Methods. 39 glucocorticoid-treated IgG4-RD patients and 22 healthy controls (HC) were enrolled. Peripheral blood mononuclear cells were separated, and circulating Th and Tfh cell subsets were examined by flow cytometry according to the surface and intranuclear markers. Disease activity was accessed by the IgG4-RD responder index (RI) score. Correlation analyses were conducted between Th/Tfh subset numbers and clinical indicators. The receiver operating characteristic (ROC) curve was used to evaluate the efficacy of Th and Tfh subsets to distinguish active IgG4-RD patients from remission IgG4-RD patients. Results. Circulating Th1, Th17, Tfh1, and Tfh17 cells were significantly increased in active IgG4-RD patients compared with HC. Th1 and Tfh1 numbers were positively correlated with serum IgG4 levels in patients with IgG4-RD. Meanwhile, the absolute numbers of circulating Th1 and Tfh1 cells were positively correlated with IgG4-RD RI scores. The areas under the curve (AUC) were 0.8276 for Th1 and 0.7310 for Tfh1, 0.5862 for Tfh2, and 0.6810 for Tfh17. Conclusion. Increased circulating Th1 and Tfh1 subsets are related to elevated serum IgG4 levels in active IgG4-RD patients during glucocorticoid treatment, which may play an important role in the course of IgG4-RD disease, and could be potential biomarkers for monitoring disease activity of IgG4-RD.