Until about 10 years ago the exact mechanisms controlling cellular response
s to the endotoxin - or lipopolysaccharide (LPS) - of Gram-negative bacteri
a were unknown. Now a considerable body of evidence supports a model where
LPS or LPS-containing particles (including intact bacteria) form complexes
with a serum protein known as LPS-binding protein; the LPS in this complex
is subsequently transferred to another protein which binds LPS, CD14. The l
atter is found on the plasma membrane of most cell types of the myeloid lin
eage as well as in the serum in its soluble form; LPS binding to these two
forms of CD14 results in the activation of cell types of myeloid and nonmye
loid lineages, respectively.