Hence, C28 has a strong capacity to block inflammatory cell accumulation in this model of allergic lung inflammation, and we also noted that this capacity was reflected by a dampening impact on the expression of important pro-inflammatory chemokines and also on Clec7a, the latter being a cell surface receptor which has been implicated as key factor in the development of asthma [30]. The gene discussed is CLEC7A; the disease is asthma.