18.11:
Transcytosis of IgG
In humans, maternal immunoglobulin G or IgG is transported from the placenta to the fetal blood through transcytosis.
IgG molecules undergo transcytosis in syncytiotrophoblasts, specialized epithelial cells of the placental villi. IgG molecules bind to FcRn receptors at the apical side of syncytiotrophoblasts.
The IgG-FcRn receptor complex is internalized through pinocytosis and sorted into a transport carrier. The transport carrier first fuses with an early endosome where the acidic environment keeps the IgG bound to the FcRn receptor.
The IgG-receptor complex is then transported through a second transport carrier to the recycling endosome. Finally, a third transport carrier delivers the IgG-receptor complex to the basolateral membrane on the fetal side of the epithelial cell.
The near-neutral pH of the basolateral membrane causes the release of the IgG from the FcRn receptor into the neonate’s bloodstream.
18.11:
Transcytosis of IgG
Transcytosis is the process in which molecules are internalized by endocytosis, transported across the cell, and released through exocytosis from the opposite end of the cell. Molecules such as insulin, immunoglobulins, and certain nutrients are transferred through the recycling endosomes by recycling and transcytosis.
IgG molecules from a mother undergo transcytosis starting around 13 weeks of gestation. The amount of IgG transferred and entering the fetal blood circulation increases with gestational age. In the process, IgG molecules cross two cellular barriers—syncytiotrophoblasts of the placental villi and the endothelial cells of the fetal capillaries.
The placental transfer of IgG from the mother to the developing fetus offers a protective advantage to both mother and fetus from infections. Specific vaccines taken during pregnancy, e.g. tetanus toxoid or inactivated influenza vaccines, elicit the production of IgG antibodies, which, after transcytosis, can potentially protect the neonate.
IgA undergoes transcytosis through the intestinal epithelial cells and is released into the intestinal lumen. IgA is produced by plasma cells as a monomer and later dimerizes. The dimeric IgA binds to the poly-IgA receptor (pIgR) at the basolateral side of the intestinal epithelial cells. The IgA-receptor complex first enters the intestinal epithelial cells through endocytosis, fuses with a recycling endosome, and is released by exocytosis at the apical end of the intestinal epithelial cells. This trajectory of IgA is opposite to that followed by IgG. In the transfer of IgG, endocytosis occurs at the apical end and exocytosis occurs at the basolateral end.
Suggested Reading
- Lamm, M. E. (1998). IV. How epithelial transport of IgA antibodies relates to host defense. American Journal of Physiology-Gastrointestinal and Liver Physiology, 274(4), G614-G617.
- Palmeira, P., Quinello, C., Silveira-Lessa, A. L., Zago, C. A., & Carneiro-Sampaio, M. (2012). IgG placental transfer in healthy and pathological pregnancies. Clinical and Developmental Immunology, 2012