Natural killer (NK) cells are critical components of host innate immunity and function as the first line of defense against tumors and viral infection. There is increasing evidence that extracellular vesicles (EVs) are involved in the antitumor activity of NK cells. NK cell-derived EVs (NKEVs) carrying cargo such as cytotoxic proteins, microRNAs, and cytokines employ multiple mechanisms to kill tumor cells, but also exhibit immunomodulatory activity by stimulating other immune cells. Several studies have reported that NKEVs can reverse immune suppression under tolerogenic conditions and contribute to NK-mediated immune surveillance against tumors. Thus, NKEVs are a promising tool for cancer immunotherapy. In this review, we describe the biological effects and potential applications of NKEVs in antitumor immunity.

Mitochondria participate in immune regulation through various mechanisms, such as changes in the mitochondrial dynamics, as metabolic mediators of the tricarboxylic acid cycle, by the production of reactive oxygen species, and mitochondrial DNA damage, among others. In recent years, studies have shown that extracellular vesicles are widely involved in intercellular communication and exert important effects on immune regulation. Recently, the immunoregulatory effects of mitochondria from extracellular vesicles have gained increasing attention. In this article, we review the mechanisms by which mitochondria participate in immune regulation and exert immunoregulatory effects upon delivery by extracellular vesicles. We also focus on the influence of the immunoregulatory effects of mitochondria from extracellular vesicles to further shed light on the underlying mechanisms.

Objective: Chemotherapy and hematopoietic stem cell transplantation (HSCT) play important roles in clinical etiology, symptoms, signs, imaging findings, and biochemical parameters for inducing posterior reversible encephalopathy syndrome (PRES) in pediatric oncologic diseases. We aimed to evaluate various risk factors of pediatric oncologic diseases after conducting chemotherapy and HSCT to induce PRES for predicting the clinical prognosis frequency. Methods: The literature was performed on PubMed, Web of Science, and Embase databases to recognize the qualified studies. The odds ratios (ORs) of related risk factors and their corresponding 95% confidence intervals (CIs) were used to compute the pooled assessments of the outcomes. Results: Six studies were included in the meta-analysis, involving 828 records. The risk of female children has a significantly higher incidence than male children in oncologic age groups of PRES. Children over the age of 10 years old in oncologic age groups develop a significantly increased risk of PRES. Acute graft-versus-host disease (GVHD) has a significant promotion effect on the occurrence of PRES. Hypertension can promote the occurrence of PRES in children. The risk of PRES in immunodeficient children increases significantly. Children with sickle cell disease (SCD) have a significantly increased risk of PRES. The risk of PRES in children with T-cell leukemia rises considerably. The central nervous system (CNS) leukemia/involvement has a significant role in promoting the occurrence of PRES in children. The pooled OR for the factors male, ≥10 years old of age, acute GVHD, hypertension, immunodeficiency, SCD, T-cell leukemia, CNS leukemia/involvement was 0.66 (95% CI: 0.58, 0.76; P