Reproductive tract inflammation is considered an important cause of male infertility. Increased leukocytes in semen can produce many reactive oxygen species (ROS), which affect sperm function. The aim of this study is to identify the main source of ROS in seminal plasma and to assess the effect of ROS on leukocytes. Semen samples ( n = 20) with leukocyte concentration >1 × 10⁶ were collected from a male infertility clinic. This study mainly compares the sperm function parameters of the normal group and the semen white blood cell group >1 × 10⁶. The results identified that ROS in semen was closely related to sperm function parameters, and CD45⁺ leucocytes were the main source of ROS. Compared with the control group, the concentration of IL-2, IL-4, IL-6, IFN-γ, and TNF-α was higher in the experimental group. Leukocytes in semen may regulate the secretion of ROS through the mammalian target of rapamycin (mTOR) pathway. A considerable amount of ROS can upregulate the expression of IL-6 in leukocytes via the nuclear factor kappa-B (NF-kB) pathway.

With the global epidemic of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the increasing number of infections, little is known about how SARS-CoV-2 affects the male reproductive system during infection or after recovery. Based on the existing research data, we reviewed the effects of SARS-CoV-2 on the male reproductive system and discussed its possible mechanism of action. SARS-CoV-2 enters host cells through the angiotensin-converting enzyme 2 (ACE2)/transmembrane serine protease 2 (TMPRSS2) pathway, and males are more susceptible than females. After infection, immunopathological damage is noticed in the testicles, and the semen index is significantly reduced. Second, abnormalities of serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) levels were also observed, suggesting that there may be dysfunction of the hypothalamic–pituitary–gonadal (HPG) axis. Even after recovery, the effect of SARS-CoV-2 on the male reproductive system can last for at least a period. There are still many unresolved questions about the effect of SARS-CoV-2 infection on the male reproductive tract. Other receptors involved during the invasion of human cells by SARS-CoV-2 remain to be identified. Will the mutation of SARS-CoV-2 increase the diversity of receptors? How does SARS-CoV-2 affect the HPG axis? The long-term effects of SARS-CoV-2 on the male reproductive system remain to be evaluated. SARS-CoV-2 infection can affect male reproductive function. Standard treatment strategies should be developed in time to protect the fertility of infected patients. For recovered patients with fertility requirements, fertility assessments should be performed and professional fertility guidance should be provided at the same time.

Despite significant advances in the diagnosis and treatment of hepatocellular carcinoma (HCC), metastasis and recurrence remain two major obstacles to improving the clinical outcomes for HCC patients. Here, we demonstrate that splenic invariant natural killer T (iNKT) cells can significantly inhibit Hepa1-6-mediated intrahepatic HCC metastasis. Interestingly, in the HCC metastasis model, iNKT deficiency can result in a significant decrease in percentage and absolute number of CD4⁺ T cell and interleukin-4 level, thus suggesting the involvement of the cross-talk between iNKTs and CD4⁺ T cells in limiting HCC metastasis to the spleen. Transcriptional signatures of CD4⁺ T cells following iNKT deficiency displaying impairment of their cell migration function. During HCC metastasis, splenic iNKT rapidly secrete interferon-γ to promote the migration of CD4⁺ T cells from the marginal zone into the white pulp, thereby triggering subsequent migration of splenic B cells to the liver and exerting anti-tumor immune effects on Hepa1-6 cells. In conclusion, interactions between interferon-γ and its receptor on iNKT and CD4⁺ T cells can effectively coordinate immune activity between the marginal zone and the white pulp, thereby ultimately inhibiting intrahepatic HCC metastasis. These findings reveal the mechanism underlying the resistance of splenic iNKT to tumor metastasis.