Rheumatoid arthritis (RA) is a systemic and heterogeneous autoimmune disease with symmetrical polyarthritis as its critical clinical manifestation. The basic cause of autoimmune diseases is the loss of tolerance to self or harmless antigens. The loss or functional deficiency of key immune cells, regulatory T (Treg) cells, has been confirmed in human autoimmune diseases. The pathogenesis of RA is complex, and the dysfunction of Tregs is one of the proposed mechanisms underlying the breakdown of self-tolerance leading to the progression of RA. Treg cells are a vital component of peripheral immune tolerance, and the transcription factor Foxp3 plays a major immunosuppressive role. Clinical treatment for RA mainly utilizes drugs to alleviate the progression of disease and relieve disease activity, and the ideal treatment strategy should be to re-induce self-tolerance before obvious tissue injury. Treg cells are one of the ideal options. This review will introduce the classification, mechanism of action, and characteristics of Treg cells in RA, which provides insights into clinical RA treatment.

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The dissolution of CO2 in brine (solubility trapping) is one of the most secure and permanent trapping mechanisms when considering CO2 geological storage. In addition, CO2 dissolution in brine is an important mechanism of CO2 enhanced oil recovery as it improves sweep efficiency and increases oil displacement. Currently, there is a range of experimental methods that has been used to measure CO2 solubility in brine and a critical review of these methods is presented here. Several different geochemical models that can be used to calculate CO2 solubility in brine are also reviewed and the importance of selecting the correct equation of state (EoS) is addressed. Furthermore, the validity of the experimental results was ascertained through a comparison of the published experimental results with those produced through geochemical modeling. The geochemical modeling software, HydraFLASH, can be used to accurately calculate CO2 solubilities under a number of conditions provided the correct EoS is selected. For the purpose of CO2‐water systems, the Valderrama‐Patel‐Teja EoS is the most accurate as it is designed to be used for systems containing polar and non‐polar compounds. The published experimental results were compared with those obtained through the geochemical modeling, to ascertain the most accurate means of measuring CO2 solubility. © 2016 Society of Chemical Industry and John Wiley & Sons, Ltd

TIGIT (T-cell immunoglobulin and ITIM domain) has emerged as a promising target in cancer immunotherapy. It is an immune “checkpoint” inhibitor primarily expressed on activated T cells, NK cells and Tregs. Engagement of TIGIT to its ligands PVR and PVR-L2 leads to inhibitory signaling in T cells, promoting functional exhaustion of tumor-infiltrating T lymphocytes. Here, we described the pre-clinical characterization of Ociperlimab (BGB-A1217), a novel humanized IgG1 anti-TIGIT antibody (mAb), and systemically evaluated the contribution of Fc functions in the TIGIT mAb-mediated anti-tumor activities. BGB-A1217 binds to the extracellular domain of human TIGIT with high affinity (KD = 0.135 nM) and specificity, and efficiently blocks the interaction between TIGIT and its ligands PVR or PVR-L2. Cell-based assays show that BGB-A1217 significantly enhances T-cell functions. In addition, BGB-A1217 induces antibody dependent cellular cytotoxicity (ADCC) against Treg cells, activates NK cells and monocytes, and removes TIGIT from T cell surfaces in an Fc-dependent manner, In vivo, BGB-A1217, either alone or in combination with an anti-PD-1 mAb elicits strong immune responses and potent anti-tumor efficacy in pre-clinical models. Moreover, the Fc effector function is critical for the anti-tumor activity of BGB-A1217 in a syngeneic human TIGIT-knock-in mouse model. The observed anti-tumor efficacy is associated with a pharmacodynamic change of TIGIT down-regulation and Treg reduction. These data support the selection of BGB-A1217 with an effector function competent Fc region for clinical development for the treatment of human cancers.