For many years, vitamin D has been acknowledged for its role in maintaining calcium and phosphate balance. However, in recent years, research has assessed its immunomodulatory role and come up with conflicting conclusions. Because the vitamin D receptor is expressed in a variety of immune cell types, study into the precise role of this molecule in diseases, notably autoimmune disorders, has been made possible. The physiologically activated version of vitamin D also promotes a tolerogenic immunological condition in addition to modulating innate and acquired immune cell responses. According to a number of recent studies, this important micronutrient plays a complex role in numerous biochemical pathways in the immune system and disorders that are associated with them. Research in this field is still relatively new, and some studies claim that patients with severe autoimmune illnesses frequently have vitamin D deficiencies or insufficiencies. This review seeks to clarify the most recent research on vitamin D’s immune system-related roles, including the pathophysiology of major disorders.

In neonatal alloimmune thrombocytopenia, almost all human platelet antigen (HPA)–1b1b mothers who produce anti–HPA-1a antibody through carrying an HPA-1a fetus are human histocompatibility leukocyte antigen (HLA)–DRB3*0101 positive. It is predicted that the HPA-1a Leu³³ polymorphism forms part of an HLA-DRB3*0101–restricted T-helper epitope, and acts as an anchor residue for binding this class II molecule. However, it is not known whether any corresponding peptides are naturally processed and presented from platelet glycoprotein. In this study, peptides displayed by a homozygous HLA-DRB3*0101 antigen-presenting cell line were identified after pulsing with recombinant HPA-1a (Leu³³ plexin-semaphorin-integrin domain). The peptides were eluted from HLA-DR molecules, fractionated by high performance liquid chromatography, and analyzed by tandem mass spectrometry. A “nested set” of naturally presented HPA-1a–derived peptides, each containing the Trp²⁵-Leu³³ core epitope, was identified, with the most abundant member being the 16-mer Met²²-Arg³⁷. These peptides may provide the basis for novel treatments to tolerize the corresponding T-helper response in women at risk of neonatal alloimmune thrombocytopenia.

Background: Multiple sclerosis along with its animal model, experimental autoimmune encephalomyelitis (EAE), are chronic inflammatory and degenerative diseases of the central nervous system (CNS). Due to the unknown cause of the disease, the most common treatments of MS are targeted for the reduction of inflammation and the repairment of CNS tissue damage, especially myelin restoration. Due to the immune protective nature of herbs, it may be useful to evaluate the impact of herbs in the diet regimen of MS patients along with their immune-mediated effects. The purpose of this study was to investigate the effect of an aqueous extract of Artemisia dracunculus (Tarragon) on the treatment of EAE in C57BL/6 mice. Methods: In this experimental study, mice were divided into the following control, untreated EAE, and A. dracunculus treated EAE groups. EAE was induced by myelin oligodendrocyte glycoprotein (MOG35-55) in female C57BL/6 mice. The symptoms of the disease and the weight of the mice were recorded daily. On day 33 after EAE induction, the mice were sacrificed and the specimens were collected. Cell proliferation and cytokine release (TGF-β, IL-17 and IL-23) from mice cultured spleen cells was measured by 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and ELISA respectively. Results: Administration of the extract of A. dracunculus mitigated EAE symptoms (P < 0.05). Furthermore, there was a reduction in the levels of inflammatory cytokines including IL-17 (P = 0.009) and IL-23 (P = 0.012) and confirmed increased serum antioxidant levels in A. dracunculus treated EAE mice (P = 0.008). Conclusions: These observations indicate that A. dracunculus extracts could reduce inflammatory cytokines and attenuate certain signs of EAE, suggesting the potential of a useful adjuvant therapy for MS.

Background and Objective: Infection by the novel coronavirus disease 2019 (COVID-19) has been associated with different types of thrombotic complications same as portal vein thrombosis (PVT). However, by emerging vaccines of COVID, the thrombosis did not seem to be concerning anymore. Until new findings showed that, the vaccine of COVID itself can cause PVT.Method: We performed an electronic search in PubMed, Scopus, and Web of Sciences to evaluate the possibility of occurring PVT due to infection and vaccination of COVID-19. The results were reported in a narrative method and categorized into tables.Result: Overall, 40 cases of PVT from 34 studies were reviewed in this article. The prevalence of PVT following COVID-19 was more remarkable in males. However, it was more common in females after vaccinations of COVID-19 in the reviewed cases. Regardless of etiology, 20 of PVT cases reviewed in this article had at least one comorbidity. The most common clinical presentation was abdominal pain (AP). After anticoagulant therapies, most of the patients improved or discharged.Conclusion: As long as the laboratory findings are not appropriate enough to predict PVT, the diagnosis of this complication with whatever underlying reason is challengeable, while rapid diagnosis and treatment of that are vital. Therefore, by providing available data in an organized way, we aimed to prepare the information of infected patients for better and easier future diagnosis of PVT in new cases.