Among the proteins highly upregulated as a consequence of interferon-stimulated transcription are the p65 GTPases (GBPs), members of the family of large GTPases that mediate resistance to intracellular pathogens. Contrary to the p47 class of GTPases, the GBPs are present in multiple copies in both the mouse and human genome.
The structure of human GBP1 has been solved and the ability of some family members to hydrolyse GTP to GDP and then to GMP is established. The antimicrobial profile of the human p65 GBPs was restricted to viruses and bacteria and few interaction partners areknown.
Human GBP1 in A549 epithelial cells restricts the replication of type II and not type I Toxoplasma and has no impact onChlamydia and Salmonella.
How does GBP1 restrict type II Toxoplasma in human cells? What Toxoplasma factors mediate the evasion of type I parasites from GBP1-driven control?