Their results suggested that polyclonal anti-GM-CSF AAbs lead to inhibition of GM-CSF through irreversible sequestration in high molecular weight immune complexes and Fc-dependent degradation, whereas therapeutic monoclonal antibody-bound GM-CSF accumulates in vivo and could dissociate and bind to its receptor, potentially preserving sufficient GM-CSF functional activity to prevent the development of PAP and susceptibility to opportunistic infection. The gene discussed is CSF2; the disease is pulmonary alveolar proteinosis.