Barnes McDowell (pagelove25)

Natural Killer (NK) cells were initially described as part of the innate immune system and characterized by their ability to lyse malignant and virus-infected cells. The cytolytic function of NK cells is tightly controlled by activating and inhibitory receptors expressed on the cell surface. Ligands that interact with a variety of NK-cell receptors include the human leukocyte antigen (HLA) molecules, and the regulation of NK-cell function by HLA class I molecules is well-established. Earlier studies also suggested a role of HLA class II molecules in regulating NK cell activity; yet, interactions between HLA class II molecules and NK cell receptors have not been well-characterized. We recently identified a subset of HLA-DP molecules that can serve as ligands for the natural cytotoxicity receptor NKp44 and activate NK cells. This novel receptor-ligand interaction provides a potential mechanism to explain the strong associations of HLA-DP molecules with HBV infection outcomes, graft-vs.-host disease and inflammatory bowel disease. Furthermore, it adds a new mechanism for NK-cell crosstalk with immune cells expressing HLA class II molecules. In this perspective article, we discuss the potential implications of NK cell receptor interactions with HLA class II molecules for the regulation of immune responses. Copyright © 2020 Niehrs and Altfeld.Stenotrophomonas maltophilia, an emerging opportunistic pathogen, is widely distributed in the environment the resistance mechanisms, and virulence factors of this bacterium facilitate its dissemination in hospitals. This study aimed to characterize the molecular epidemiology of S. maltophilia strains associated with an outbreak in the Children's Hospital of México Federico Gómez (HIMFG). Twenty-one clinical S. maltophilia strains were recovered from cultures of blood and urine samples from 10 pediatric patients at the emergency department, and nine environmental S. maltophilia strains recovered from faucets in the same area were also included. Two of the 10 patients were related with health care-associated infections (HCAIs), and the other eight patients (8/10) were infected with environmental S. maltophilia strains. The outbreak was controlled by monthly disinfection of the faucets in the emergency department. Typing using pulsed-field gel electrophoresis (PFGE) showed a 52% genetic diversity with seven pulains isolated from blood most strongly adhered to HTB-9 cells. In conclusion, the molecular epidemiology and some of the features such as resistance, and virulence genes associated with colonization patterns are pathogenic attributes that can promote S. maltophilia dissemination, persistence, and facilitate the outbreak that occurred in the HIMFG. This study supports the need for faucet disinfection as a control strategy for clinical outbreaks. Copyright © 2020 Cruz-Córdova, Mancilla-Rojano, Luna-Pineda, Escalona-Venegas, Cázares-Domínguez, Ormsby, Franco-Hernández, Zavala-Vega, Hernández, Medina-Pelcastre, Parra-Ortega, Rosa-Zamboni, Ochoa and Xicohtencatl-Cortes.There is no effective cure for Chagas disease, which is caused by infection with the arthropod-borne parasite, Trypanosoma cruzi. In the search for new drugs to treat Chagas disease, potential therapeutic targets have been identified by exploiting the differences between the mechanisms involved in intracellular Ca2+ homeostasis, both in humans and in trypanosomatids. In the trypanosomatid, intracellular Ca2+ regulation requires the concerted action of three intracellular organelles, the endoplasmic reticulum, the single unique mitochondrion, and the acidocalcisomes. The single unique mitochondrion and the acidocalcisomes also play central roles in parasite bioenergetics. At the parasite plasma membrane, a Ca2+--ATPase (PMCA) with significant differences from its human counterpart is responsible for Ca2+ extrusion; a distinctive sphingosine-activated Ca2+ channel controls Ca2+ entrance to the parasite interior. Several potential