Wikipedia

Thirumala-Devi Kanneganti

Thirumala-Devi Kanneganti is an immunologist and is the Rose Marie Thomas Endowed Chair, Vice Chair of the Department of Immunology, and Member at St. Jude Children's Research Hospital.[1] She is also Director of the Center of Excellence in Innate Immunity and Inflammation at St. Jude Children's Research Hospital. Her research interests include investigating fundamental mechanisms of innate immunity, including inflammasomes and inflammatory cell death, PANoptosis, in infectious and inflammatory disease and cancer.[1]

Thirumala-Devi Kanneganti
Born
Kothagudem, India
Alma mater
Known for
Awards
Scientific career
FieldsImmunology
InstitutionsSt. Jude Children's Research Hospital
Websitehttps://www.stjude.org/kanneganti

Early life and education edit

Kanneganti is from Kothagudem, Telangana (United Andhra Pradesh), India. 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 then received her M.Sc. and PhD from Osmania University in India.[3]

Career edit

Kanneganti began her career in research as a PhD student studying plant pathogens and fungal toxins.[4] She then went on to do postdoctoral fellowships at the University of Wisconsin and the Ohio State University studying fungal genetics and plant innate immunity.[2][3] She transitioned to study mammalian innate immunity at the University of Michigan.[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.[1][3] She was promoted to a full Member in 2013. She became Vice Chair of the Immunology Department in 2016 and was endowed with the Rose Marie Thomas Endowed Chair in 2017.[5] In 2022, she also became the Director of the Center of Excellence in Innate Immunity and Inflammation at St. Jude.[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.[1][6][7][8][9][10]

Awards and honors edit

  • American Association of Immunology-BD Biosciences Investigator Award (2015)[11]
  • Vince Kidd Memorial Mentor of the Year Award (2015)[1]
  • Society for Leukocyte Biology Outstanding macrophage researcher Dolph O. Adams Award (2017)[12][13]
  • American Society for Microbiology Eli Lilly and Company-Elanco Research Award (2017)[13]
  • Interferon and Cytokine Research Seymour & Vivian Milstein Award for Excellence (2018)[1][4]
  • Clarivate/Web of Science list of Highly Cited Researchers (2017, 2018, 2019, 2020, 2021, 2022, 2023)[1][6][7][8][9][10]
  • NIH R35 Outstanding Investigator Award (2020)[14][15]
  • Fellow in the American Academy of Microbiology, American Society for Microbiology (2021)[16]
  • Outstanding Scientist Award, AAIS in Cancer Research (2022)[17]
  • Rosalind Franklin Society Special Award in Science (2023)[18]
  • Fellow in the American Association for the Advancement of Science (AAAS) (2023)[19]
  • American Association of Immunology-Thermo Fisher Meritorious Career Award (2024)[20]

Major contributions edit

Discovery of NLRP3 inflammasome, ZBP1-, RIPK1-, AIM2-, and NLRP12-PANoptosomes, and PANoptosis as therapeutic targets for infectious and inflammatory diseases and cancer edit

Kanneganti is well known for her breakthrough discoveries elucidating the functions of innate immune receptors, inflammasomes, and inflammatory cell death and for making fundamental contributions to inflammasome biology and the cell death field.[21][22][23][24][25] Her studies, along with those from other groups published in 2006, provided the first genetic evidence for the role of NLRP3 in the formation of the inflammasome, caspase-1 activation, and IL-1β/IL-18 maturation.[26][27] These initial studies showed that microbial components,[21][28][29] ATP,[30][31] and MSU crystals[32] activate the NLRP3 inflammasome.

Kanneganti discovered that Influenza A virus, Candida, and Aspergillus specifically activate the NLRP3 inflammasome and elucidated the physiological role of the NLRP3 inflammasome in host defense.[21][33][34][35][36][37] Beyond infectious diseases, her lab also established the importance of the NLRP3 inflammasome in autoinflammatory diseases,[38] intestinal inflammation,[39] neuroinflammation,[40] cancer,[14] and metabolic diseases.[41]

Kanneganti's lab has also worked on the upstream regulatory mechanisms of NLRP3 and inflammasome-induced inflammatory cell death, pyroptosis. Her lab identified caspase-8 and FADD as expression and activation regulators of both the canonical and non-canonical NLRP3 inflammasome/pyroptosis.[42] Her group also characterized redundancies between caspase-1 and caspase-8 and between NLRP3 and caspase-8 in autoinflammatory disease and linked diet and the microbiome to these processes.[38][43][44] These studies demonstrated that the NLRP3 inflammasome/pyroptotic pathway is closely connected to the caspase-8–mediated programmed cell death pathway.[38][42][43][44] This finding went against the dogma that existed at that time that caspase-8 and FADD were involved only in apoptosis.[42]

Following up on her original discovery that NLRP3 senses viral RNAs,[28] her lab discovered Z-DNA binding protein 1 (ZBP1)/DAI as an innate immune sensor of influenza virus upstream of the NLRP3 inflammasome and cell death; however, this cell death was not consistent with any of the cell death pathways characterized at that time.[22][45] This led Kanneganti to characterize ZBP1 as a regulator of PANoptosis, a unique innate immune inflammatory cell death pathway driven by caspases and RIPKs that is regulated by multiprotein PANoptosome complexes.[46] The multifaceted PANoptosome complexes have been visualized in single cells to integrate several molecular components, including ASC, caspase-8, and RIPK3.[47][48][49][50][51][52][53]

She then went on to establish that multiple PANoptosomes can contain different sensors and respond to different triggers:

  • The ZBP1-PANoptosome responds to influenza virus infection[22][49][54]
  • The RIPK1-PANoptosome responds to Yersinia infection and the inhibition of transforming growth factor beta-activated kinase 1 (TAK1), a molecule Kanneganti identified as a master regulator that maintains cellular homeostasis by negatively regulating the NLRP3 inflammasome and inflammatory cell death[47]
  • The AIM2-PANoptosome responds to Francisella and herpes simplex virus 1 infections[55][51]
  • The NLRP12-PANoptosome responds to the combination of heme and PAMPs or TNF[56][57]

Collectively, these studies identified ZBP1, AIM2, RIPK1, NLRP12, TAK1, and caspase-8 as master molecular switches of inflammasome activation and PANoptosis. Additionally, her group discovered that interferon regulatory factor 1 (IRF1), a critical regulator of inflammation and cell death,[58] regulates the activation of PANoptosis.[59]

PANoptosis is implicated in driving innate immune responses and inflammation. Kanneganti's research group has also further elucidated the molecular mechanisms of PANoptosis and showed that the enigmatic caspase-6 is critical for ZBP1-mediated NLRP3 inflammasome activation, PANoptosis, innate immune responses, and host defense against influenza virus.[49] Her lab also showed that coronavirus activates PANoptosis and that inhibiting the NLRP3 inflammasome or gasdermin D during coronavirus infection increases cell death and cytokine secretion rather than decreasing them.[60] Her research group also recently discovered the role of NINJ1, a key executioner of inflammatory cell death, in mediating PANoptosis following heat stress and infection, thereby identifying NINJ1 and PANoptosis effectors as potential therapeutic targets.[61]

Her group has also discovered the role of PANoptosis in cytokine storm, identifying TNF and IFN-γ as key cytokines that cause this inflammatory cell death pathway and lead to lung damage, organ failure, and lethality. Kanneganti's research group also showed that inhibiting TNF and IFN-γ could prevent lethality in SARS-CoV-2 infection, septic shock, hemophagocytic lymphohistiocytosis, and cytokine shock in mice.[62] This led her to advocate for the evaluation of a strategy to repurpose approved drugs that inhibit TNF-α or IFN-γ, as well as those that target other molecules in the PANoptosis pathway (e.g., JAK), to prevent the cytokine storm and pathogenesis.[62][63] Additional work in Kanneganti's lab focusing on beta-coronaviruses showed that IFN induces ZBP1-mediated PANoptosis, which causes morbidity and mortality. These findings led her team to suggest that inhibiting ZBP1 may improve the efficacy of IFN therapy for COVID-19 and impact other infectious and inflammatory diseases where IFNs cause pathology.[64][46]Beyond infectious disease and inflammatory syndromes, Kanneganti's group has also found that activating PANoptosis could be beneficial to eliminating cancer cells. Treatment of cancer cells with PANoptosis-inducing agents TNF and IFN-γ can reduce tumor size in preclinical models.[62][65][66] 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.[48][67]

Overall, work from Kanneganti's lab has implicated PANoptosis in infectious, metabolic, hemolytic, neurologic, and autoinflammatory diseases and cancer.[22][38][47][48][49][62][46][56]

Cytokine signaling and disease edit

Kanneganti's lab showed compensatory roles for NLRP3/caspase-1 and caspase-8 in the regulation of IL-1β production in osteomyelitis.[43][44] Additionally, discoveries from her research group suggest that IL-1α and IL-1β can have distinct roles in driving inflammatory disease.[68] She identified the role of the IL-1α and RIPK1/TAK1/SYK signaling pathways in skin inflammation.[68] Furthermore, her studies also showed the role of another IL-1 family member, IL-33, in regulating immune responses and microbiota in the gut.[69] 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.[70][43][68][69][71]

Beyond her studies on IL-1 family members, her recent work on cytokine storm established TNF and IFN-γ as the key upstream cytokines that cause inflammatory cell death (PANoptosis), tissue and organ damage, and mortality, and she has suggested that strategies to target these cytokines or other molecules in their signaling pathway should be evaluated as therapeutic strategies in COVID-19, sepsis, and other diseases associated with cytokine storm.[62]

References edit

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