Among the few available studies, Todt, et al. [19] observed that active smoking, (independent of COPD stage) reduces both the percent of lung macrophages expressing TLR3 and poly I:C-induced CXCL10 production in vitro, without altering other endosomal or cytoplasmic receptors such as TLR7/8/9, RIG-I, MDA-5 or PKR, so that positive numbers of TLR3-macrophages directly correlated with lung function. The gene discussed is TLR3; the disease is chronic obstructive pulmonary disease.