Conversely, blocking Clec5a with monoclonal antibodies, before infection with Dengue or Japanese encephalitis viruses in mice, reduced the secretion of proinflammatory cytokines such as TNF and IL-6, as well as the activation of NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes in mice; this restored homeostasis and led to resolution of infection, suggesting that blocking of Clec5a might potentially alleviate tissue damage and protect against some viral infections [135,136]. This evidence concerns the gene CLEC5A and dengue disease.