T cell-produced interferon ɣ (IFN ɣ) during course of infection also effected augmented FcɣR levels on alveolar macrophages which in turn stimulated IFN ɣ production by secretion of inflammatory cytokines (interleukin (IL)-18, IL-12), linking innate and adaptive immunity in a positive feedback loop. The gene discussed is IFNA1; the disease is infection.