The observation that direct interaction of d7EB and CD11bϩ cells was required for the anti-inflammatory phenotype of CD11bϩ cells led to consideration of the involvement of NO, an important inflammatory mediator of sepsis, 25 in the response. A time course study of NO production in cultured d7EBs over 6 hours demonstrated that d7EB cells constitutively produced NO and that they also strongly expressed eNOS ( Figure 5, A  and B) .