Netspot nuclear medicine 3 vials skin#

Chronic urticaria, defined as urticaria that persists for >6 wk, occurs in 0.1% of the population ( 2), and in a significant percentage of cases (∼40–80%), there is no identifiable cause ( 1, 3).

Urticaria, or hives, is a common disease that can affect up to 20% of the general population ( 1).

Netspot nuclear medicine 3 vials skin#

Our findings implicate MCs as IL-1β producers in the skin and mediators of histamine-independent urticaria through the NLRP3 inflammasome. Furthermore, MCs expressing disease-associated but not wild-type NLRP3 secreted IL-1β and induced neutrophil migration and vascular leakage, the histological hallmarks of urticarial rash, when transplanted into mouse skin. Primary MCs expressed inflammasome components and secreted IL-1β via NLRP3 and apoptosis-associated speck-like protein containing a caspase recruitment domain when stimulated with microbial stimuli known to activate caspase-1. Unlike normal MCs that required stimulation with proinflammatory stimuli for IL-1β production, resident MCs from CAPS patients constitutively produced IL-1β. We identified mast cells (MCs) as the main cell population responsible for IL-1β production in the skin of CAPS patients. However, the cellular mechanisms regulating IL-1β production in the skin of CAPS patients remain unclear. Urticarial rash observed in cryopyrin-associated periodic syndrome (CAPS) caused by nucleotide-binding oligomerization domain–leucine-rich repeats containing pyrin domain 3 (NLRP3) mutations is effectively suppressed by anti–interleukin (IL)-1 treatment, suggesting a pathophysiological role of IL-1β in the skin.