Only a very low level of GM-CSF is beneficial.

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By contrast, GM-CSF is barely detectable in the blood of healthy individuals and is thought to serve less of a role in homeostatic myelopoiesis, as evidenced by the fact that GM-CSF-deficient mice have a virtually normal lifespan and have less dramatic alterations in the basal myeloid system,

Importantly, however, GM-CSF is known to be a critical homeostatic factor in lung alveoli, where it is produced at low levels for the development and long-term maintenance of alveolar macrophages. Severe deficiency of GM-CSF (for example, due to autoantibodies to GM-CSF or mutations that ablate GM-CSFR function) causes pulmonary alveolar proteinosis (PAP), a life-threatening interstitial lung disease in which dysfunctional alveolar macrophages cannot clear surfactant

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