This contrasts with the results obtained using peritoneal macrophages from TLR-4-deficient (C3H/HeJ) and control mice (C3H/HePas) infected with S. schenckii yeast cells, where significantly greater amounts of pro-inflammatory mediators, such as NO and TNF-α (early-stage post-infection), and anti-inflammatory cytokines, such as IL-10 (late-stage post-infection), were produced by thioglycollate-elicited peritoneal macrophages from infected C3H/HePas mice [58]. The gene discussed is TNF; the disease is infection.