Steven Antony Krilis
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| Steven Antony Krilis AM | |
|---|---|
| Born | 26 November 1947 Athens, Greece |
| 🏫 Education | University of New South Wales; University of Sydney; Harvard Medical School |
| 💼 Occupation | |
| Known for | Research on beta-2 glycoprotein I, antiphospholipid syndrome, and the Sydney classification criteria |
| 🏅 Awards | Member of the Order of Australia; Corresponding Member of the Academy of Athens; honorary doctorate, National and Kapodistrian University of Athens |
Steven Antony Krilis AM (born 26 November 1947) is a Greek-born Australian physician-scientist, clinical immunologist and academic. He is a conjoint professor in the School of Clinical Medicine at the University of New South Wales (UNSW) and has served as head of the Department of Infectious Disease, Immunology and Sexual Health at St George Hospital, Sydney.[1]
His research has addressed antiphospholipid syndrome (APS), beta-2 glycoprotein I (β2GPI), thrombosis, allergy, inflammation, innate immunity and the redox regulation of extracellular plasma proteins.[1]
Early life and education
Krilis was born in Athens, Greece, on 26 November 1947.
He studied medicine at the University of New South Wales, graduating with honours, and completed a PhD at the University of Sydney. He subsequently became a Fellow of the Royal Australasian College of Physicians.[1]
His doctoral work concerned the biochemical characterisation of house-dust-mite allergens and developed his expertise in protein chemistry and immunochemistry.
Supported by an Australian National Health and Medical Research Council fellowship and a Fogarty International Postdoctoral Research Fellowship, Krilis undertook postdoctoral research at Harvard Medical School and Brigham and Women's Hospital.[1]
Working with K. Frank Austen and Elias J. Corey, he investigated sulfidopeptide leukotrienes.
Academic career
Krilis returned to Australia and developed an academic and clinical career at the University of New South Wales and St George Hospital, Sydney. The official citation accompanying his appointment as a Member of the Order of Australia records that he became Director of the Department of Immunology, Allergy and Infectious Diseases at St George Hospital in 1988 and was appointed Professor in the St George Hospital Clinical School in 1992.[2]
The department subsequently became the Department of Infectious Disease, Immunology and Sexual Health.[1]
His laboratory combined clinical immunology with biochemical, molecular and animal-model studies and supervised doctoral students, clinician-scientists and postdoctoral researchers. He established long-term collaborations with research groups in Europe, North America and Asia, including the National and Kapodistrian University of Athens and the Biomedical Research Foundation of the Academy of Athens.[3]
Throughout his career, Krilis has combined clinical practice in clinical immunology with laboratory-based research into thrombosis, autoimmunity, inflammation and extracellular protein redox biology. His work has integrated protein chemistry, structural biology, immunology and animal models to investigate the biological functions of β2-glycoprotein I and their relevance to autoimmune and thrombotic disease.
Research
Leukotriene biology
During his Harvard postdoctoral work, Krilis contributed to studies of sulfidopeptide leukotrienes. In 1984, Krilis, Lewis, Corey and Austen reported a specific high-affinity receptor for leukotriene C4 in guinea-pig ileal smooth muscle and associated membrane fractions. The receptor's binding characteristics were consistent with mediation of the contractile response to leukotriene C4.[4]
Mast-cell biology
After returning to Australia, Krilis established a programme in human mast-cell biology. His laboratory investigated the differentiation and maturation of mast cells from human bone-marrow progenitors and factors regulating mast cells and basophils.[5][6]
β2-glycoprotein I and antiphospholipid syndrome
In 1989, Krilis and colleagues reported that autoimmune anticardiolipin-antibody binding depended on a plasma cofactor.[7] In 1990, they purified the cofactor and identified it as β2GPI, also known as apolipoprotein H.[8] Subsequent work from the laboratory investigated the structure, ligand binding and biological functions of β2GPI.
Structure and gene-targeted mice
The laboratory used mutagenesis and structural studies to identify regions of β2GPI involved in phospholipid binding, including basic residues in domain V.[9]
In 2001, Krilis and colleagues reported the first published gene-targeted β2GPI-deficient mouse model. Plasma from the deficient mice showed impaired thrombin generation.[10]
Haemostasis and vascular injury
Krilis and colleagues showed that β2-glycoprotein I binds coagulation factor XI and inhibits its activation by thrombin and factor XIIa.[11] The interaction was localised to domain V, which is cleaved by factor XIa.[12]
The group subsequently demonstrated redox regulation of the interaction between β2-glycoprotein I and von Willebrand factor by thioredoxin-1.[13] Domain V mediated the antithrombotic activity of β2-glycoprotein I in murine thrombosis models.[14]
Innate immunity
Experimental studies demonstrated that β2-glycoprotein I ameliorates Gram-negative bacterial inflammation and protects mice against Gram-negative septicaemia.[15][16]
Extracellular protein redox biology
Krilis and colleagues investigated extracellular thiol-disulphide exchange in circulating plasma proteins. Their studies demonstrated redox regulation of β2-glycoprotein I, coagulation factor XI and other plasma proteins, and developed assays for free-thiol angiotensinogen as a biomarker for pre-eclampsia.[17][18][19]
International leadership and classification criteria
Krilis organised and chaired the 11th International Congress on Antiphospholipid Antibodies in Sydney in 2004. The associated international workshop produced the revised APS classification criteria published in 2006, widely known as the Sydney classification criteria.[20]
Reviews
Krilis has co-authored several widely cited reviews on antiphospholipid syndrome and β2-glycoprotein I, including How I Treat the Antiphospholipid Syndrome (Blood, 2009), The Pathogenesis of the Antiphospholipid Syndrome (New England Journal of Medicine, 2013), and a 2024 review of β2-glycoprotein I domain V in Clinical Immunology.[21][22][23]
Honours and recognition
Krilis was appointed a Member of the Order of Australia (AM) in the 2019 Queen's Birthday Honours for significant service to medical research.[2]
He received an honorary doctorate from the National and Kapodistrian University of Athens in 2011 and was elected a Corresponding Member of the Academy of Athens in 2023.[24][3]
Selected publications
- McNeil, H. P.; Chesterman, C. N.; Krilis, S. A. (1989). "Anticardiolipin antibodies and lupus anticoagulants comprise separate antibody subgroups with different phospholipid binding characteristics". British Journal of Haematology.
- McNeil, H. P.; Simpson, R. J.; Chesterman, C. N.; Krilis, S. A. (1990). "Anti-phospholipid antibodies are directed against a complex antigen that includes β2-glycoprotein I". Proceedings of the National Academy of Sciences of the United States of America.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 "Conjoint Professor Steven Krilis". University of New South Wales. Retrieved 16 July 2026.
- ↑ 2.0 2.1 "Queen's Birthday 2019 Honours List: Member (AM) in the General Division of the Order of Australia, A–L" (PDF). Governor-General of Australia. 10 June 2019. Retrieved 16 July 2026.
- ↑ 3.0 3.1 "Greek Australian Steve Krilis elected member of the Academy of Athens". The Greek Herald. 3 May 2023. Retrieved 16 July 2026.
- ↑ Krilis, S.; Lewis, R. A.; Corey, E. J.; Austen, K. F. (1984). "Specific binding of leukotriene C4 to smooth muscle cells and evidence for a high-affinity receptor". Proceedings of the National Academy of Sciences of the United States of America. 81 (14): 4529–4533. PMC 345643. PMID 6087330.
- ↑ Li, L.; Meng, X. W.; Krilis, S. (1996). "Mast cells expressing chymase but not tryptase can be derived by culturing human progenitors in conditioned medium obtained from a human mastocytosis cell strain with c-kit ligand". Journal of Immunology. 156 (12): 4839–4844. PMID 8648136.
- ↑ Li, L.; Krilis, S. A. (1999). "Mast-cell growth and differentiation". Allergy. 54 (4): 306–312. doi:10.1034/j.1398-9995.1999.00086.x. PMID 10371088.
- ↑ Cite error: Invalid
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<ref>tag; no text was provided for refs namedMcNeil1990 - ↑ Sheng, Y. H.; Sali, A.; Herzog, H.; Lahnstein, J.; Krilis, S. A. (1996). "Site-directed mutagenesis of recombinant human β2-glycoprotein I identifies a cluster of lysine residues that are critical for phospholipid binding and anticardiolipin antibody cofactor activity". Journal of Immunology. 157 (8): 3744–3751. PMID 8871678.
- ↑ Sheng, Y.; Reddel, S. W.; Herzog, H.; Wang, Y. X.; Brighton, T.; France, M. P.; Robertson, S. A.; Krilis, S. A. (2001). "Impaired thrombin generation in β2-glycoprotein I null mice". Journal of Biological Chemistry. 276 (17): 13817–13823. doi:10.1074/jbc.M010990200.
- ↑ Shi, T.; Iverson, G. M.; Qi, J. C.; Cockerill, K. A.; Linnik, M. D.; Konecny, P.; Krilis, S. A. (2004). "Beta 2-glycoprotein I binds factor XI and inhibits its activation by thrombin and factor XIIa: loss of inhibition by clipped beta 2-glycoprotein I". Proceedings of the National Academy of Sciences of the United States of America. 101 (11): 3939–3944. doi:10.1073/pnas.0400281101. PMC 374359. PMID 15007174.
- ↑ Shi, T.; Giannakopoulos, B.; Iverson, G. M.; Cockerill, K. A.; Linnik, M. D.; Krilis, S. A. (2005). "Domain V of beta2-glycoprotein I binds factor XI/XIa and is cleaved at Lys317-Thr318". Journal of Biological Chemistry. 280 (2): 907–912. doi:10.1074/jbc.M410291200. PMID 15522884.
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External links
Category:1947 births
Category:Living people
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