Severe Acute Respiratory Syndrome (SARS), Middle East Respiratory Syndrome (MERS), and Coronavirus Disease 2019 (COVID-19) infections are the three epidemiological diseases caused by the Coronaviridae family. Perceiving the immune responses in these infections and the escape of viruses could help us design drugs and vaccines for confronting these infections. This review investigates the innate and adaptive immune responses reported in the infections of the three coronaviruses SARS, MERS, and COVID-19. Moreover, the present study can trigger researchers to design and develop new vaccines and drugs based on immune system responses. In conclusion, due to the need for an effective and efficient immune stimulation against coronavirus, a combination of several strategies seems necessary for developing the vaccine.

Background Endometriosis is a chronic and relatively common disease in women of childbearing age. Complications of this disease include a wide range of disorders. The cause of this disease is not known for sure, but several hypotheses have been proposed for it. Aim In this review, an attempt has been made to discuss the effects of oxidative stress on various complications of endometriosis. Content In endometriosis, the entry of endometrial tissues into the peritoneal cavity causes oxidative stress through the Fenton reaction and inflammation in this site. Fenton reaction can produce reactive oxygen species through a catalytic form of iron. This process can provoke inflammatory responses and oxidative injury. As a result, the activity of macrophages and expression of nuclear factor‐kappa B increase. Oxidative stress can be associated with many complications of endometriosis. It has been reported that in the peritoneal fluid of endometriosis patients, there are activated macrophages, growth factors, and high concentrations of cytokines. These conditions act as a toxic to embryo survival and sperm function. Implications Novel therapeutic strategies must regulate intracellular ROS signaling to inhibit the adverse effects of ROS‐induced endometriosis‐promoting events. According to features of antioxidants, they may inhibit early events of the development of endometriosis.

Background Endometriosis is a chronic inflammatory disease associated with the growth and proliferation of endometrial‐like tissues outside the uterus. Although the exact etiology and mechanism of the pathogenesis of the disease have not been fully elucidated, the immune system cells and the mediators produced by them can be named as effective factors in the onset and progression of the disease. Aims We aim to attempt to review studies on the role of the immune system in endometriosis to better understand the pathogenesis of endometriosis. Content Abundant production of inflammatory mediators by neutrophils and macrophages and reduced cytotoxicity of defined cells promote endometriosis at the early stages of the disease. Following an increase in the inflammation of the environment, the body takes compensatory mechanisms to reduce inflammation and establish homeostasis. For this purpose, the body produces remodeling and anti‐inflammatory factors leading to slow conversion of the inflammatory environment into a non‐inflammatory environment with proliferative and immunosuppressive properties. Environmental conditions induce M2 macrophages, TH2 cells, and Tregs differentiation, promoting disease progression by producing angiogenic and immunosuppressive factors. However, the exact molecular mechanism involved in changing inflammatory to non‐inflammatory conditions is not yet fully understood. Implications Due to the common characteristics of endometriotic cells and cancer cells, most potential treatment options for endometriosis have been suggested due to the results of these methods in the treatment of cancer. In this pathway, immune system cells and soluble mediators can be used as targets.