Recent experimental work in rodents has demonstrated that the liver can function as an 'IgA-pump', transporting polymeric IgA from serum to bile via a secretory-component mediated uptake at the surface of the hepatic parenchymal cell. Studies are surveyed which indicate that, although this process occurs in man, it is to a strikingly lesser degree, and interruption of this pathway does not explain the high serum IgA levels often seen in chronic liver disease: the explanation for this lies in enhanced synthesis of IgA, and diminished polymeric IgA catabolism unrelated to hepatobiliary transport.
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H. J. F. Hodgson (1985) studied this question.
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