| First Author | Yilmaz B | Year | 2014 |
| Journal | Cell | Volume | 159 |
| Issue | 6 | Pages | 1277-89 |
| PubMed ID | 25480293 | Mgi Jnum | J:219215 |
| Mgi Id | MGI:5619891 | Doi | 10.1016/j.cell.2014.10.053 |
| Citation | Yilmaz B, et al. (2014) Gut microbiota elicits a protective immune response against malaria transmission. Cell 159(6):1277-89 |
| abstractText | Glycosylation processes are under high natural selection pressure, presumably because these can modulate resistance to infection. Here, we asked whether inactivation of the UDP-galactose:beta-galactoside-alpha1-3-galactosyltransferase (alpha1,3GT) gene, which ablated the expression of the Galalpha1-3Galbeta1-4GlcNAc-R (alpha-gal) glycan and allowed for the production of anti-alpha-gal antibodies (Abs) in humans, confers protection against Plasmodium spp. infection, the causative agent of malaria and a major driving force in human evolution. We demonstrate that both Plasmodium spp. and the human gut pathobiont E. coli O86:B7 express alpha-gal and that anti-alpha-gal Abs are associated with protection against malaria transmission in humans as well as in alpha1,3GT-deficient mice, which produce protective anti-alpha-gal Abs when colonized by E. coli O86:B7. Anti-alpha-gal Abs target Plasmodium sporozoites for complement-mediated cytotoxicity in the skin, immediately after inoculation by Anopheles mosquitoes. Vaccination against alpha-gal confers sterile protection against malaria in mice, suggesting that a similar approach may reduce malaria transmission in humans. |
