Nonetheless, it may still be notable that several TH1 and other pro-inflammatory mediators which initiate or amplify immune responses (e.g., IL-1β, IL-6, TNF-α, G-CSF) were comparatively over-produced by the IPF CD4+CD28null cells relative to their autologous CD4+CD28+ counterparts, both constitutively, and with TCR stimulation (Figure 2). The gene discussed is IL1B; the disease is idiopathic pulmonary fibrosis.