She received her undergraduate degree from Singareni Collieries Women's College, Kothagudem at Kakatiya University, where she majored in chemistry, zoology, and botany.
[2][3] She joined St. Jude Children's Research Hospital as an Assistant Member in the Immunology Department in 2007, where she has focused on studying inflammasomes and cell death.
[5] Kanneganti is among the most "Highly Cited Researchers" in the world due to the noteworthy impact of her findings in the fields of innate immunity, inflammation, and cell death.
[46][47] PANoptosomes are multi-protein complexes assembled by germline-encoded pattern-recognition receptor(s) (PRRs) (innate immune sensor(s)) in response to pathogens, including bacterial, viral, and fungal infections, as well as pathogen-associated molecular patterns, damage-associated molecular patterns, cytokines, and homeostatic changes during infections, inflammatory conditions, and cancer.
[22][38][48][49][50][51][52][53][54][55][56][57][58][59] She then went on to establish that multiple PANoptosomes can contain different sensors and respond to different triggers: Collectively, these studies identified ZBP1, AIM2, RIPK1, NLRP12, TAK1, and caspase-8 as master molecular switches of inflammasome activation and PANoptosis.
Kanneganti's research group identified the ZBP1-PANoptosome as crucial for host defense during influenza A virus infections, revealing its role in promoting inflammatory cell death.
Additionally, her lab discovered that the AIM2-PANoptosome mediates PANoptosis during Francisella novicida infections [61] Her work has extended to bacterial pathogens Salmonella enterica and Listeria monocytogenes, where the loss of caspases and RIPK3 offers protection against cell death.
[68] Beyond infectious disease and inflammatory syndromes, Kanneganti's group has also found that activating PANoptosis could be beneficial to eliminating cancer cells.
[51][56][55] Her group also discovered a regulatory relationship between ADAR1 and ZBP1 that can be targeted with the combination of nuclear export inhibitors, such as selinexor, and IFN to drive ZBP1-mediated PANoptosis and regress tumors in preclinical models.
Her research identified that NLCR5- and NLRP12-mediated PANoptosis is activated by heme, which can be released during red blood cell lysis in infections or inflammatory diseases.
[71] Overall, Kanneganti's lab discovered distinct and previously unrecognized functions of the cytokines IL-1α, IL-1β, and IL-33 and their signaling pathways in inflammatory diseases and cancer.