Honors & Awards

  • T32 Postdoctoral Trainee, NIH NIDDK; Stanford School of Medicine, Department of Pediatrics, Division of Hematology/Oncology (02/01/2021 - Present)

Professional Education

  • Doctor of Philosophy (PhD), University of California, Merced, Immunoparasitology (2020)
  • Master of Health Science (MHS), Quinnipiac University, Biomedical Sciences (2014)
  • Bachelor of Science (BS), University of California, Los Angeles, Biochemistry (2009)

Stanford Advisors

Lab Affiliations

All Publications

  • Naive CD8 T cell IFN gamma responses to a vacuolar antigen are regulated by an inflammasome-independent NLRP3 pathway andToxoplasma gondiiROP5 PLOS PATHOGENS Kongsomboonvech, A. K., Rodriguez, F., Diep, A. L., Justice, B. M., Castallanos, B. E., Camejo, A., Mukhopadhyay, D., Taylor, G. A., Yamamoto, M., Saeij, J. J., Reese, M. L., Jensen, K. C. 2020; 16 (8): e1008327


    Host resistance to Toxoplasma gondii relies on CD8 T cell IFNγ responses, which if modulated by the host or parasite could influence chronic infection and parasite transmission between hosts. Since host-parasite interactions that govern this response are not fully elucidated, we investigated requirements for eliciting naïve CD8 T cell IFNγ responses to a vacuolar resident antigen of T. gondii, TGD057. Naïve TGD057 antigen-specific CD8 T cells (T57) were isolated from transnuclear mice and responded to parasite-infected bone marrow-derived macrophages (BMDMs) in an antigen-dependent manner, first by producing IL-2 and then IFNγ. T57 IFNγ responses to TGD057 were independent of the parasite's protein export machinery ASP5 and MYR1. Instead, host immunity pathways downstream of the regulatory Immunity-Related GTPases (IRG), including partial dependence on Guanylate-Binding Proteins, are required. Multiple T. gondii ROP5 isoforms and allele types, including 'avirulent' ROP5A from clade A and D parasite strains, were able to suppress CD8 T cell IFNγ responses to parasite-infected BMDMs. Phenotypic variance between clades B, C, D, F, and A strains suggest T57 IFNγ differentiation occurs independently of parasite virulence or any known IRG-ROP5 interaction. Consistent with this, removal of ROP5 is not enough to elicit maximal CD8 T cell IFNγ production to parasite-infected cells. Instead, macrophage expression of the pathogen sensors, NLRP3 and to a large extent NLRP1, were absolute requirements. Other members of the conventional inflammasome cascade are only partially required, as revealed by decreased but not abrogated T57 IFNγ responses to parasite-infected ASC, caspase-1/11, and gasdermin D deficient cells. Moreover, IFNγ production was only partially reduced in the absence of IL-12, IL-18 or IL-1R signaling. In summary, T. gondii effectors and host machinery that modulate parasitophorous vacuolar membranes, as well as NLR-dependent but inflammasome-independent pathways, determine the full commitment of CD8 T cells IFNγ responses to a vacuolar antigen.

    View details for DOI 10.1371/journal.ppat.1008327

    View details for Web of Science ID 000566549000005

    View details for PubMedID 32853276

    View details for PubMedCentralID PMC7480859