- Metabolic reprogramming of CD8+ T cells in chronic inflammatory diseases
- Research Associate, Department of Immunology and Inflammation, Imperial College London
- Ph.D., Department of Paediatrics and Adolescent Medicine, The University of Hong Kong
- MPhil, Department of Surgery, The University of Hong Kong
- B.Sc., (Hons), Department of Biochemistry, The University of Hong Kong
Sustained inflammation causes immune cell dysfunction and forms the common pathological basis for many chronic inflammatory diseases including chronic viral infection, cancer and autoimmunity. A key aspect of immune cell dysfunction that underpins the clinical outcome of these chronic conditions is the development of exhausted CD8+T cells. Nonetheless, reasons for CD8+T cell exhaustion remain incompletely understood. Our laboratory employs the emerging technologies from the field of immunometabolism to assess the effects of sustained inflammation on exhausted T cell differentiation and population diversity. Our long-term goal is to develop metabolism-targeting drugs to regulate T cell immunity in infection, cancer and autoimmunity.
- Buang N, Tapeng L, Gray V, Sardini A, Chad W, Lightstone L, Cairns T, Pickering M, Behmoaras J, Ling GS*, Botto M*. Type I interferons affect the metabolic fitness of CD8+T cells from patients with systemic lupus erythematosus. Nature Communications 2021 12:1980 doi: 10.1038/s41467-021-22312-y *Joint corresponding author
- Ling GS, Crawford G, Buang N, Bartok I, Tian K, Thielens NM, Bally I, Harker JA, Ashton-Rickardt PG, Rutschmann S, Strid J, Botto M. C1q restrains autoimmunity and viral infection by regulating CD8+ T cell metabolism. Science 2018 Vol 360:558-563.
- Ling GS*, Bulla R*, Tripodo C*, Rami D*, Agostinis C, Guarnotta C, Zorzet S, Durigutto P, Botto M, Tedesco F. C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation. Nature Communications 2016 Feb 1;7:10346. doi: 10.1038/ncomms10346. *Joint first author
- Barbour TD, Ling GS, Ruseva MM, Fossati-Jimack L, Cook HT, Botto M, Pickering MC. Complement receptor 3 mediates renal protection in experimental C3 glomerulopathy. Kidney International 2016 Vol 89(4):823-32.
- Carlucci F, Ishaque A, Ling GS, Szajna M, Sandison A, Donatien P, Cook HT, Botto M. C1q modulates the response to TLR7 stimulation by pristane-primed macrophages: implications for pristane-induced lupus. Journal of Immunology 2016 Vol 196(4):1488-94.
- Fossati-Jimack L, Ling GS, Baudino L, Szajna M, Manivannan K, Zhao JC, Midgley R, Chai JG, Simpson E, Botto M, Scott D. Intranasal peptide-induced tolerance and linked suppression: consequences of complement deficiency. Immunology 2015 Vol 144(1):149-57.
- Ling GS, Bennett J, Woollard KJ, Szajna M, Fossati-Jimack L, Taylor PR, Scott D, Franzoso G, Cook HT, Botto M. Integrin CD11b positively regulates TLR4-induced signalling pathways in dendritic cells but not in macrophages. Nature Communications 2014;5:3039. doi: 10.1038/ncomms4039
- Ling GS*, Sattler S*, Xu D, Hussaarts L, Romaine A, Zhao H, Fossati-Jimack L, Malik T, Cook HT, Botto M, Lau YL, Smits HH, Liew FY, Huang FP. IL-10-producing regulatory B cells induced by IL-33 (BregIL-33) effectively attenuate mucosal inflammatory responses in the gut. Journal of Autoimmunity 2014 Vol 50:107-22. *Joint first author
- Bossi F, Tripodo C, Rizzi L, Bulla R, Agostinis C, Guarnotta C, Munaut C, Baldassarre G, Papa G, Zorzet S, Ghebrehiwet B, Ling GS, Botto M, Tedesco F. C1q as a novel player in angiogenesis with therapeutic implication in wound healing. Proceedings of National Academy of Science of the United States of America 2014 Vol 111(11):4209-14.
- Ling GS*, Fossati-Jimack L*, Cortini A, Szajna M, Malik TH, McDonald JU, Pickering MC, Cook HT, Taylor PR, Botto M. Phagocytosis is the main CR3-mediated function affected by the lupus-associated variant of CD11b in human myeloid cells. PLOS One 2013 Vol 8: e57082 *Joint first author
- Ling GS, Cook HT, Botto M, Lau YL, Huang FP. An essential protective role of IL-10 in the immunological mechanism underlying resistance vs. susceptibility to lupus induction by dendritic cells and dying cells. Rheumatology 2011 Vol 50: 1773-84.
- 2015: The Department of Medicine teaching award, Imperial College London
Last updated: October 30, 2019