Résumé
B / T lymphuocyte attenuator (BTLA) is one of the important checkpoint molecules in immune regulation. BTLA belongs to the CD28 superfamily, and its protein structure is similar to programmed cell death-1 (PD-1) and cytotoxic T lymphocyte associated antigen-4 (CTLA-4). BTLA is mainly expressed in B and T cells, and has also been found in some innate immune cells such as dendritic cells and monocytes. To date, the herpesvirus entry mediator (HVEM) is the only ligand for BTLA found in human cells. HVEM belongs to the Tumor necrosis factor receptor (TNFR) superfamily, and its interaction with BTLA directly connects CD28 and TNFR families. The binding of BTLA with HVEM often mediates immunosuppressive effects and plays an important role in maintaining immune tolerance. However, recent studies have found that the BTLA / HVEM pathway not only provides negative regulatory signals, but also promotes the survival of T cells. This bidirectional signaling system renders BTLA-mediated immune regulation more sophisticated and complex. Growing evidence has shown that BTLA is involved in T cells, B cells and dendritic cell-mediated immune regulation, and therefore plays an important role in a variety of immune related diseases, such as inflammation, tumor, infectious diseases and autoimmune diseases. Based on the latest research progress at home and abroad, this paper reviews the role of BTLA in immune regulation and immune related diseases.
Résumé
There are a wide variety of gastrointestinal microbiota, and the total number of bacteria reached 100 trillion. The flora interacts with the human body, and has a great impact on human health. In recent years, the relationship between intestinal flora and human diseases has become a hot research at home and abroad. Many studies have shown that intestinal microbiome plays an important role in modulating risk of multiple systemic diseases, including digestive system diseases, metabolic diseases, neuropsychiatric diseases, immune-related diseases and tumors.In this paper, the relationship between intestinal flora and human diseases was reviewed and summarized. The research progress on the relationship between gastrointestinal microbiota and human diseases in recent five years was summarized, which provided new ideas for the diagnosis and treatment of human diseases.
Résumé
Background: PTPN22 codifies for a protein-tyrosine-phosphatase (Lyp) involved in T cell receptor signaling regulation. p53 is involved in immune related inflammation regulating STAT 1 and pro-inflammatory cytokines. Possible interaction between the two systems concerning the susceptibility to immune related disorders are therefore biologically plausible. In the present note we have searched for such interaction in type 1 diabetes mellitus and reviewed previous data from our laboratory. Methods: We have studied 287 children with type 1 diabetes, 129 non diabetic adult subjects admitted to the Hospital for Coronary Artery Disease, 130 women with endometriosis and 256 healthy blood donors. PTPN22 and p53 codon 72 genotypes were determined by DNA analysis. Results: In all diseases the proportion of PTPN22 *T allele is higher in p53 *Pro allele carriers than in p53*Arg/*Arg genotype. In *Arg/*Arg patients the proportion of *T allele carriers does not differ significantly from controls while in subjects carrying the *Pro allele is higher in patients than in controls. A significant increase of Odds Ratio is observed only in presence of both *T and *Pro alleles suggesting a cooperative interaction. Conclusion: It has been suggested that the susceptibility to autoimmune disorders in the presence of *T allele could be related to failure to delete auto reactive T cell during intrathymic selection. *Pro allele variant with its strong transcriptional activity could enhance the multiplication of such auto reactive T cell escaping intrathymic thus explaining a significant increase of Odds Ratio in the presence of both factors .The present observation could have relevance to identify individuals at high risk of clinical manifestations.