Butyrophilin-3A (BTN3A) subfamily members are a group of immunoglobulins present on the surface of different cell types, including innate and cancer cells. Due to their high similarity with the B7 family members, different studies have been conducted and revealed the involvement of BTN3A molecules in modulating T cell activity within the tumor microenvironment (TME). However, a great part of this research focused on γδ T cells and how BTN3A contributes to their functions. In this review, we will depict the roles and various aspects of BTN3A molecules in distinct tumor microenvironments and review how BTN3A receptors modulate diverse immune effector functions including those of CD4+ (Th1), cytotoxic CD8+ T cells, and NK cells. We will also highlight the potential of BTN3A molecules as therapeutic targets for effective immunotherapy and successful cancer control, which could represent a bright future for patient treatment.

BackgroundNonsyndromic cleft lip with or without cleft palate (NSCL/P) is one of the most common craniofacial malformations observed. Several studies suggest that the decrease in folate has been associated with a higher risk of NSCL/P. The present study aimed to determine the association of 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism gene with the occurrence of NSCL/P in the Moroccan population.MethodsMTHFR C677T was genotyped in 52 Moroccan patients and 182 unrelated controls, using a PCR followed by restriction fragment length polymorphism.ResultsThe results of the study revealed a genotypic and phenotypic distribution in equilibrium with Hardy–Weinberg’s law (χ2=0.36, P=0.55). The frequency of heterozygous genotype C/T and the T allele in controls and patients were 40.7% vs 15.4% and 26%, respectively.ConclusionA low association was found between the C677T polymorphism of the MTHFR gene and a risk for the development of NSCL/P in the Moroccan population (OR =0.24, P=0.0005).

Background: Diffuse glioma is a malignant human brain cancer that is hard to overcome. This represents a high risk of mortality. The current challenge is limited to the control of tumor progression and survival improvement.Immunotherapy consists of stimulating the immune system in order to eliminate the non-self-elements that damage the human body, including cancer cells. However, in human glioma, the current immunotherapeutic targets did not show significant benefit. In this study, we aimed at evaluating the expression and potential role of a new immunosuppressive molecule, TIGIT in glioma patients. Patients and Methods: A cohort of 667 patients from the TCGA database along with a cohort of 53 Moroccan patients, were analyzed in order to assess the role of TIGIT in human glioma progression and to estimate whether blocking this immune checkpoint molecule would be of a potential therapeutic benefit.Real time RT-PCR from fresh human biopsies and bioinformatics approaches were both used in this study. Results: Our results showed that high expression of TIGIT had prognostic value with some known clinical glioma risk factors such as sex, age and mutation status. High expression of TIGIT was positively associated with an advanced grade of glioma. Moreover, elevated levels of TIGIT were correlated to higher rates of FoxP3, a regulatory T-cell marker that reflects a strong immunosuppressive microenvironment. Interestingly, TIGIT showed strong association with Treg cell-secreted cytokines (TGF-beta and IL-10), supporting the likely involvement of TIGIT in the exhaustion of the intra-tumoral immune cells. Finally, elevated rates of TIGIT were significantly associated to elevated rates of other inhibitory immune checkpoint molecules (PD-1, VISTA and Tim-3) in human glioma patients.Conclusions: TIGIT blockade might be of valuable therapeutic benefit in patients with advanced gliomas.