Interferon and IL-27 Antagonize the Function of Group 2 Innate Lymphoid Cells and Type 2 Innate Immune Responses Scientists found that tissue-resident group 2 innate lymphoid cells (ILC2 cells) proliferated in situ without migrating during inflammatory responses. Both type I and type II interferons and interleukin 27 (IL-27) suppressed ILC2 function in a manner dependent on the transcription factor STAT1. [Nat Immunol] Abstract | Press Release Type I Interferon Restricts Type 2 Immunopathology through the Regulation of Group 2 Innate Lymphoid Cells Researchers found that deficiency in signaling via type I interferon receptor led to deregulated activation of group 2 innate lymphoid cells and infection-associated type 2 immunopathology. [Nat Immunol] Abstract Trastuzumab Emtansine (T-DM1) Renders HER2+ Breast Cancer Highly Susceptible to CTLA-4/PD-1 Blockade Investigators showed that drug resistance can be overcome with trastuzumab emtansine, an antibody-drug conjugate that combines the human epidermal growth factor receptor 2 (HER2)-targeting ability of trastuzumab with a cytotoxic drug, which the antibody delivers directly to the tumor. [Sci Transl Med] Abstract | Press Release Neutrophil-Derived Microvesicles Enter Cartilage and Protect the Joint in Inflammatory Arthritis Neutrophils play an active role in protecting cartilage from damage by dispatching microvesicles (MVs) to do their bidding in this tissue they otherwise can’t access. In two different mouse models of rheumatoid arthritis, MVs delivered locally entered the cartilage, prevented the loss of proteoglycans, and maintained cartilage integrity. [Sci Transl Med] Abstract | Press Release PDL1 Regulation by p53 via miR-34 Investigators confirmed that PDL1 is a direct target of miR-34 with western blotting and luciferase assays and used a syngeneic mouse model to deliver miR-34a–loaded liposomes plus radiotherapy and assessed PDL1 expression and tumor-infiltrating lymphocytes. [J Natl Cancer Inst] Abstract | Press Release Autophagy Is Dispensable for B-Cell Development but Essential for Humoral Autoimmune Responses Scientists showed that autophagy is dispensable for pro- to pre-B cell transition, but necessary at a basal level to maintain normal numbers of peripheral B cells. It appears non-essential for B-cell activation under B-cell receptor stimulation but required for their survival after lipopolysaccharide stimulation that drives plasmablast differentiation and for specific IgM production after immunization. [Cell Death Differ] Abstract PPARγ Antagonist Attenuates Mouse Immune-Mediated Bone Marrow Failure by Inhibition of T Cell Function To examine the role of adipocytes in bone marrow failure, researchers investigated peroxisomal proliferator-activated receptor gamma, a key transcription factor in adipogenesis, utilizing an antagonist of this factor called bisphenol-A-diglycidyl-ester. In vitro, bisphenol-A-diglycidyl-ester suppressed activation and proliferation, and reduced phospholipase C gamma 1 and nuclear factor of activated T-cells 1 expression, as well as inhibited calcium flux in T cells. [Haematologica] Abstract | Full Article A Novel Cyclic Helix B Peptide Inhibits Dendritic Cell Maturation during Amelioration of Acute Kidney Graft Rejection through Jak-2/STAT3/SOCS1 Scientists investigated the effects of cyclic helix B peptide (CHBP) on dendritic cells (DCs) in a rat renal transplantation model. Five successive treatment doses of CHBP after transplantation significantly ameliorated acute rejection with lower histological injury, apoptosis and CD4+ and CD8+ T-cell infiltration in renal allografts. [Cell Death Dis] Full Article Don’t forget to subscribe to Human Immunology News and Immunology of Infectious Disease News! |