Immunodeficiency: UNC-93B gets a toll call.
Defects in innate immunity have moved to center stage in the past five years. This can be explained, at least in part, by the development of molecular assays and genetic tools that enable new approaches. Two recent studies using these elegant tools show that a transmembrane endoplasmic reticulum protein, UNC-93B, is essential for the normal response to signaling through the Toll-like receptors (TLRs) that respond to viral infection, TLR3, TLR7, TLR8 and TLR9.
Conley
Mary Ellen
ME
Department of Pediatrics, University of Tennessee College of Medicine, Memphis, TN 38103, USA. maryellen.conley@stjude.org
D000818:Animals; D004198:Disease Susceptibility; D006801:Humans; D007113:Immunity, Innate; D007153:Immunologic Deficiency Syndromes / Q000209:etiology*; D026901:Membrane Transport Proteins / Q000172:deficiency / Q000502:physiology*; D051379:Mice; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000502:physiology*; D014777:Virus Diseases / Q000276:immunology
D026901:Membrane Transport Proteins; D051193:Toll-Like Receptors; C454130:UNC93B1 protein, human