However, certain aspects of LPS-mediated effects on cytokine secretion in T cells via TLR4 in vitro did not fully correlate with the pattern seen in vivo: TLR4 signaling in CD4+ T cells was shown to be inhibitory in a spontaneous model of colitis (48), whereas Reynolds et al. demonstrated that TLR4 signaling promoted the development of experimental autoimmune encephalomyelitis (EAE) in mice (49). The gene discussed is TLR4; the disease is experimental autoimmune encephalomyelitis.