Cameron et al [20] demonstrated that IL-18 is constitutively expressed in the airway epithelium and parenchyma of murine lung tissue and human bronchial biopsies and that its expression is increased under conditions characterized by Th1 cytokine expression such as lipopolysaccharide stimulation and pulmonary sarcoidosis and reduced during Th2 cytokine-mediated conditions such as ovalbumin challenge and asthma. This evidence concerns the gene IL18 and asthma.