The lung lymphocytes were predominantly CD4+ T cells, with numerous CD8+ T cells, natural killer cells, and γδ T cells.32 In another study upregulation of IL-17A was associated with the development of experimental silicosis, but was markedly reduced in athymic, γδ T cell-deficient or CD4+ T cell-depleted mice. The gene discussed is CD4; the disease is silicosis.