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The Journal of Immunology, 2003, 170: 3528-3533.
Copyright © 2003 by The American Association of Immunologists

The MHC Class I-Like IgG Receptor Controls Perinatal IgG Transport, IgG Homeostasis, and Fate of IgG-Fc-Coupled Drugs1

Derry C. Roopenian2,*, Gregory J. Christianson*, Thomas J. Sproule*, Aaron C. Brown*, Shreeram Akilesh*, Nadja Jung*, Stefka Petkova*, Lia Avanessian*, Eun Young Choi*, Daniel J. Shaffer*, Peter A. Eden* and Clark L. Anderson{dagger}

* The Jackson Laboratory, Bar Harbor, ME 04609; and {dagger} Ohio State University, Columbus, OH 43210

Abs of the IgG isotype are efficiently transported from mother to neonate and have an extended serum t1/2 compared with Abs of other isotypes. Circumstantial evidence suggests that the MHC class I-related protein, the neonatal FcR (FcRn), is the FcR responsible for both in vivo functions. To understand the phenotypes imposed by FcRn, we produced and analyzed mice with a defective FcRn gene. The results provide direct evidence that perinatal IgG transport and protection of IgG from catabolism are mediated by FcRn, and that the latter function is key to IgG homeostasis, essential for generating a potent IgG response to foreign Ags, and the basis of enhanced efficacy of Fc-IgG-based therapeutics. FcRn is therefore a promising therapeutic target for enhancing protective humoral immunity, treating autoimmune disease, and improving drug efficacy.


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