Transcription factor B-cell lymphoma/leukemia 11A (BCL11A) gene encodes a zinc-finger protein that is predominantly expressed in brain and hematopoietic tissue. BCL11A functions mainly as a transcriptional repressor that is crucial in brain, hematopoietic system development, as well as fetal-to-adult hemoglobin switching. The expression of this gene is regulated by microRNAs, transcription factors and genetic variations. A number of studies have recently shown that BCL11A is involved in β-hemoglobinopathies, hematological malignancies, malignant solid tumors, 2p15-p16.1 microdeletion syndrome, and type II diabetes. It has been suggested that BCL11A may be a potential prognostic biomarker and therapeutic target for some diseases. In this review, we summarize the current research state of BCL11A, including its biochemistry, expression, regulation, function and its possible clinical application in human diseases.

Cancer immunotherapy enhances the body's immunity against tumors by mitigating immune escape. Compared with traditional chemotherapy, immunotherapy has the advantages of fewer drugs, a wider range of action and fewer side effects. B7-H7 (also known as HHLA2, B7y) is a member of the B7 family of costimulatory molecules that was discovered more than 20 years ago. B7-H7 is mostly expressed in organs such as the breast, intestine, gallbladder and placenta and is detected predominantly in monocytes/macrophages in the immune system. Its expression is upregulated after stimulation by inflammatory factors such as lipopolysaccharide and interferon-γ. B7-H7/transmembrane and immunoglobulin domain containing 2 (TMIGD2) and killer cell immunoglobulin-like receptor, three Ig domains and long cytoplasmic tail 3 (KIR3DL3)-B7-H7 are the two currently confirmed signaling pathways for B7-H7. An increasing number of studies have demonstrated that B7-H7 is widely present in a variety of human tumor tissues, especially in programmed cell death-1 (PD-L1)-negative human tumors. B7-H7 promotes tumor progression, disrupts T-cell-mediated antitumor immunity, and inhibits immune surveillance. B7-H7 also triggers tumor immune escape and is associated with clinical stage, depth of tumor infiltration, metastasis, prognosis, and survival related to different tumor types. Multiple studies have shown that B7-H7 is a promising immunotherapeutic target. Herein, review the current literature on the expression, regulation, receptors and function of B7-H7 and its regulation/function in tumors.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is one of the most frequent types of autoimmune encephalitis. However, the instigating mechanisms are as yet not fully ascertained. Cardinal clinical manifestations of anti-NMDAR encephalitis include acute behavioural change, psychosis, and catatonia. As the level of diagnosis increases, encephalitis becomes more common, but there are never been published in patients with anti-NMDAR encephalitis and simultaneous hypertrophic pachymeningitis. A sixty-eight-year-old man who presented with mental, behavioral abnormalities, unstable walking, headaches, and erratic hand movements. The neuropsychiatric symptoms and cerebrospinal fluid examination was consistent with the diagnosis criteria of anti-NMDAR encephalitis. Magnetic resonance imaging of the brain showed a thickening of dura mater localized at the left tentorium cerebelli, left cerebral hemisphere, and cerebral falx; the thickening dura mater was characterized by an intense contrast enhancement after the administration of gadolinium. High doses of intravenous methylprednisolone were administrated during his hospitalization. After 5 days, the patient’s condition improved. We herein describe a rare case of a 68-year-old man with anti-NMDAR encephalitis presenting with concomitant hypertrophic pachymeningitis. We systematically expounded anti-NMDAR encephalitis and hypertrophic pachymeningitis, and made bold conjectures on the etiology and pathogenesis of these two diseases, hoping to stimulate new ideas from clinicians and basic medical researchers.

Glioblastoma is the most malignant primary glioma. Conventional treatment methods that include surgery, radiotherapy, and chemotherapy have a limited curative effect on the tumor. With the deepening of molecular biology research, molecular targeted therapy has opened a new era of tumor therapy. Programmed death ligand 1 (PD-L1) has been proved to play a pivotal role in the tumor immune evasion process. Previous studies have confirmed the specific expression of PD-L1 in glioblastoma tissues and cells, but there are few studies on inflammation regulating PD-L1 in glioblastoma. In this study, real-time PCR, flow cytometry, and western blot were applied to detect PD-L1 in glioblastoma cells. Short hairpin RNA was used to knock down PD-L1 in glioblastoma cells. Cell counting kit-8 experiment and wound-healing assay were used to detect the proliferation and migration of glioblastoma cells. Here we demonstrated that PD-L1 was overexpressed in glioblastoma cells, and interferon-gamma (IFN-γ) induces PD-L1 in glioblastoma cells via activating p38/JNK/ERK signaling pathways. To summarize, PD-L1 promotes the occurrence and development of glioblastoma. IFN-γ counteracts the tumor-promoting effects mediated by PD-L1 in glioblastoma. IFN-γ regulates PD-L1 through multiple signaling pathways, but the total effect of IFN-γ-mediated inflammatory signals still need to be further explored in glioblastoma. PD-L1 enhances the proliferation and migration of glioblastoma cells by regulating CDK4, CDK6, MMP-2, and vimentin molecules. Most importantly, targeting PD-L1 can be applied in the treatment of glioblastoma. We speculate that IFN-γ may affect glioblastoma through other pathways, and we will continue to further explore the mechanisms in the future.