We recently published an article describing the importance of CXCL17 in T cell responses [1]. In summary, we observed the following:
1) Cxcl17 is necessary to maintain normal ratios of T cell subpopulations in lymph nodes (LN).
2) Cxcl17-/- mice develop more intense inflammatory responses than wild type mice.

In the past decade, a tremendous progress has been made in developing T cell engaging bi-specific antibodies (BsAbs) targeting CD19 to treat B cell malignancies. The T cell engaging bi-specific molecule binds to CD3 on a T cell and a tumor-associated antigen (TAA) on a target cell and redirects the T cell to a specific target cell bypassing the MHC restriction mechanism, leading to the formation of immune synapse between the T cell and target cell and target cell lysis.

Since Gershon and Kondo’s initial description of suppressor T cells as antigen-specific T cells that regulate immune responses [1], several advances have taken place on the biology and potential applications of regulatory T cells (Tregs) in clinical settings. After that, Sakaguchi et al. identified Treg cells capable of protecting lymphopenic mice against autoimmune disease produced by neonatal thymectomy [2], and Morrissey et al.

The promising results of immune checkpoint inhibitors (ICIs) in tumors have changed the current treatment modality for cancer. ICIs response prediction is urgently needed for the personalized therapy approach. In the recent issue of the Journal of Oncology, Zixin Hu et al. proposed that DNA methylation alternations contribute to tumor microenvironment (TME) reshapement to predict the ICIs response. Notwithstanding the global DNA methylation loss, the repression of T cell receptor signaling and the fellow costimulators by DNA hypermethylation contributed to the cold TME and ICIs resistance.

Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease.