Objective To investigate the death of chondrocytes in rats which feed with T-2 toxin under selenium (Se) deficient conditions.Methods Thirty two healthy male SD rats were divided into two groups by weight which were normal diet group and Se deficiency diet group,16 rats in each group.Rats in normal diet group were fed with Se 101.5 μg/kg diet,and rats in Se deficiency diet group were fed with Se 1.1 μg/kg diet for 30 d.Normal diet group was divided into control group and T-2 toxin group,and Se deliciency diet group was randomly divided into Se-deficiency group and Se-deficiency plus T-2 toxin group,8 rats in each group.After that,rats in T-2 toxin and Se-deficiency plus T-2 toxin groups were administrated intragastrically with T-2 toxin (100 μg/kg) everyday for 30 d.Rats were put to death,the left knee was taken and stained with hematoxylin-eosin and SafraninFast green,pathological changes of rat's knee joint cartilage were observed under light microscopy,expression levels of active caspase-3 and receptor interacting protein 3 (RIP3) in rat's articular cartilage cells were determined via the immunohistochemical method.The apoptosis was also detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL).Results Red ghost outlines of chondrocyte and multiple chondral cell clusters surrounded the non-cell areas in deep zone of articular cartilage of knee joint stained with hematoxylineosin were seen in Se-deficiency plus T-2 toxin group under light microscope.In the superficial zone of cartilage,the positive percent of TUNEL and active caspase-3 in Se-deficiency plus T-2 toxin group was higher than those of control group,Se-deficiency group and T-2 toxin group [(7.47-± 0.34)％ vs (4.68 ± 0.54)％,(2.67-± 0.64)％,(2.56 ±0.54)％;(4.75 ± 0.67)％ vs (1.24 ± 0.25)％,(0.00 ± 0.00)％,(0.00 ± 0.00)％,P ＜ 0.05].In the middle zone of cartilage,the positive percent of TUNEL,active caspase-3 and RIP3 in Se-deficiency plus T-2 toxin group was significantly higher than those of control group,T-2 toxin group and Se-deficiency group [(72.06 ± 6.15)％ vs (16.10 ± 3.00)％,(19.57 ± 3.49)％,(19.33 ± 5.19)％;(51.13 ± 4.18)％ vs (10.97-± 3.01)％,(15.36 ± 4.37)％,(15.23 ± 3.13)％;(25.91 ± 13.39)％ vs (1.59 ± 1.14)％,(4.32 ± 2.91)％,(7.50 ± 5.00)％,P ＜ 0.05].The positive percents of TUNEL,active caspase-3 and RIP3 were not significantly different in the deep zone (P ＞ 0.05).Conclusion The death of the middle zone in the rat cartilage induced by T-2 toxin under selenium deficient conditions isapoptosis and necroptosis.

Xenotransplantation is an efficient pathway to solve the problem of transplant organ source deficiency in clinical settings. With the increasing progress of gene editing technique and immune suppression regimen, important development has been achieved on researches regarding pig to non-human primate kidney xenotransplantation, which provides a good condition for the introduction of the technique in the clinical application. In view of the substantial difference between human and non-human primate, and to meet the needs of current ethic requirements, it is necessary to perform subclinical studies for pig to human kidney xenotransplantation. In recent years, such subclinical studies with regard to the genetically modified pig to brain death recipient kidney xenotransplantation had been performed, indicating that kidney xenotransplantation gradually began to transit to the clinical development stage. However, donor/recipient selection and immune suppression regimen has not reached a consensus yet, and has to be clarified in subclinical studies. In this article, the current status and confronted problems of donor/recipient selection, immune suppression regimen and post transplantation management in the subclinical studies of kidney xenotransplantation were reviewed, aiming to promote the clinical transformation of kidney xenotransplantation to the clinical application.

CD47 is a transmembrane protein widely expressed on cell surface, which is considered as a key molecule for immune escape. With an increasing number of related studies, the role of CD47 and its ligands in immunomodulatory effects has been gradually understood. Recent studies have investigated the role of CD47 in ischemia-reperfusion injury of allogenetic kidney transplantation, rejection and xenotransplantation. Nevertheless, the specific role and the key mechanism remain elusive. In this article, the structure and function of CD47, common CD47 ligands, the relationship between CD47 and kidney transplantation, and the application of CD47 in kidney transplantation were reviewed, the latest research progress of CD47 in kidney transplantation was summarized, and the limitations of current research and subsequent research direction were analyzed, aiming to provide reference for subsequent application of CD47 in allogeneic and kidney xenotransplantation.