Biology ETDs

Publication Date

Summer 7-14-2021


Toxoplasma gondii is a pathogen whose control partly depends upon Toll-like receptors (TLR) 11 and 12, that signal through MyD88. Yet, human TLR11 and TLR12 are nonfunctional, motivating us to investigate MyD88-independent immune pathways. Parasite dense granule protein GRA24 activates p38 MAPK independently of MyD88 in macrophages. Using wild-type and GRA24-deleted T. gondii strains, I demonstrate GRA24 activates p38 MAPK, resulting in IL-12 production, and protective immunity. Furthermore, GRA24 triggers p38 MAPK-dependent CX3CL1 production. GRA24 also induces CCL17 and Ppbp independently of p38 MAPK. Additionally, I demonstrate GRA24 downregulates CCL12. Furthermore, IL-15 is negatively regulated by GRA24 through activation of p38 MAPK activation. Moreover, I show GRA24 may play a role in CD4+ T cell recruitment during T. gondii infection. Together, this research is a prime example of the fine balance of inflammatory events triggered by T. gondii to ensure persistence of both host and parasite.




Toxoplasma gondii, Myd88, GRA24, dense granule protein

Document Type


Degree Name


Level of Degree


Department Name

UNM Biology Department

First Committee Member (Chair)

Dr. Eric Y. Denkers

Second Committee Member

Dr. Irene Salinas

Third Committee Member

Dr. Eric S. Loker

Fourth Committee Member

Dr. David J. Bzik

Included in

Biology Commons