Search

Your search keyword '"Jones, Gareth W."' showing total 12 results
Start Over Author "Jones, Gareth W." Publication Year Range Last 3 years
12 results on '"Jones, Gareth W."'

1. IL-27 maintains cytotoxic Ly6C+ γδ T cells that arise from immature precursors

Author

Wiesheu, Robert, Edwards, Sarah C, Hedley, Ann, Hall, Holly, Tosolini, Marie, Fares da Silva, Marcelo Gregorio Filho, Sumaria, Nital, Castenmiller, Suzanne M, Wardak, Leyma, Optaczy, Yasmin, Lynn, Amy, Hill, David G, Hayes, Alan J, Hay, Jodie, Kilbey, Anna, Shaw, Robin, Whyte, Declan, Walsh, Peter J, Michie, Alison M, Graham, Gerard J, Manoharan, Anand, Halsey, Christina, Blyth, Karen, Wolkers, Monika C, Miller, Crispin, Pennington, Daniel J, Jones, Gareth W, Fournie, Jean-Jacques, Bekiaris, Vasileios, and Coffelt, Seth B

Published
2024
Full Text
View/download PDF

3. Author Reply to Peer Reviews of IL-27 maintains cytotoxic Ly6C+ gamma delta T cells that arise from immature precursors

Author

Wiesheu, Robert, primary, Edwards, Sarah C., additional, Hedley, Ann, additional, Tosolini, Marie, additional, Fares da Silva, Marcelo Gregorio Filho, additional, Sumaria, Nital, additional, Optaczy, Yasmin, additional, Hill, David G., additional, Hayes, Alan J., additional, Hay, Jodie, additional, Kilbey, Anna, additional, Michie, Alison M., additional, Graham, Gerry, additional, Manoharan, Anand, additional, Halsey, Christina, additional, Jones, Gareth W, additional, Blyth, Karen, additional, Fournie, Jean-Jacques, additional, Pennington, Dan, additional, Bekiaris, Vasileios, additional, and Coffelt, Seth B., additional

Published
2023
Full Text
View/download PDF

4. IL-27 maintains cytotoxic Ly6C+ gamma delta T cells that arise from immature precursors

Author

Wiesheu, Robert, primary, Edwards, Sarah C., additional, Hedley, Ann, additional, Tosolini, Marie, additional, Fares da Silva, Marcelo Gregorio Filho, additional, Sumaria, Nital, additional, Optaczy, Yasmin, additional, Hill, David G., additional, Hayes, Alan J., additional, Hay, Jodie, additional, Kilbey, Anna, additional, Michie, Alison M., additional, Graham, Gerry, additional, Manoharan, Anand, additional, Halsey, Christina, additional, Jones, Gareth W, additional, Blyth, Karen, additional, Fournie, Jean-Jacques, additional, Pennington, Dan, additional, Bekiaris, Vasileios, additional, and Coffelt, Seth B., additional

Published
2023
Full Text
View/download PDF

5. Th1 Cells Alter the Inflammatory Signature of IL-6 by Channeling STAT Transcription Factors to Alu-like Retroelements

Author

Millrine, David, primary, Cardus Figueras, Ana, additional, Uceda Fernandez, Javier, additional, Andrews, Robert, additional, Szomolay, Barbara, additional, Cossins, Benjamin C., additional, Rice, Christopher M., additional, Li, Jasmine, additional, Tyrrell, Victoria J., additional, McLeod, Louise, additional, Holmans, Peter, additional, O’Donnell, Valerie B., additional, Taylor, Philip R., additional, Turner, Stephen J., additional, Jenkins, Brendan J., additional, Jones, Gareth W., additional, Topley, Nicholas, additional, Williams, Nigel M., additional, and Jones, Simon A., additional

Published
2023
Full Text
View/download PDF

6. Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity

Author

Jenkins, Benjamin J., primary, Blagih, Julianna, additional, Ponce-Garcia, Fernando M., additional, Canavan, Mary, additional, Gudgeon, Nancy, additional, Eastham, Simon, additional, Hill, David, additional, Hanlon, Megan M., additional, Ma, Eric H., additional, Bishop, Emma L., additional, Rees, April, additional, Cronin, James G., additional, Jury, Elizabeth C., additional, Dimeloe, Sarah K., additional, Veale, Douglas J., additional, Thornton, Catherine A., additional, Vousden, Karen H., additional, Finlay, David K., additional, Fearon, Ursula, additional, Jones, Gareth W., additional, Sinclair, Linda V., additional, Vincent, Emma E., additional, and Jones, Nicholas, additional

Published
2023
Full Text
View/download PDF

8. Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity

Author

Jenkins, Benjamin J, Blagih, Julianna, Ponce-Garcia, Fernando M, Canavan, Mary, Gudgeon, Nancy, Eastham, Simon, Hill, David, Hanlon, Megan M, H, Eric, Bishop, Emma L, Rees, April, Cronin, James G, Jury, Elizabeth C, Dimeloe, Sarah K, Veale, Douglas J, Thornton, Catherine A, Vousden, Karen H, Finlay, David K, Fearon, Ursula, Jones, Gareth W, Sinclair, Linda V, Vincent, Emma E, and Jones, Nicholas

Subjects
Signalling & Oncogenes, Metabolism, Cell Biology
Abstract

Augmented T cell function leading to host damage in autoimmunity is supported by metabolic dysregulation, making targeting immunometabolism an attractive therapeutic avenue. Canagliflozin, a type 2 diabetes drug, is a sodium glucose co-transporter 2 (SGLT2) inhibitor with known off-target effects on glutamate dehydrogenase and complex I. However, the effects of SGLT2 inhibitors on human T cell function have not been extensively explored. Here, we show that canagliflozin-treated T cells are compromised in their ability to activate, proliferate, and initiate effector functions. Canagliflozin inhibits T cell receptor signaling, impacting on ERK and mTORC1 activity, concomitantly associated with reduced c-Myc. Compromised c-Myc levels were encapsulated by a failure to engage translational machinery resulting in impaired metabolic protein and solute carrier production among others. Importantly, canagliflozin-treated T cells derived from patients with autoimmune disorders impaired their effector function. Taken together, our work highlights a potential therapeutic avenue for repurposing canagliflozin as an intervention for T cell-mediated autoimmunity.

Published
2023
Full Text
View/download PDF

10. Th1 cells alter the inflammatory signature of IL-6 by channeling STAT transcription factors toAlu-like retroelements

Author

Millrine, David, primary, Figueras, Ana Cardus, additional, Fernandez, Javier Uceda, additional, Andrews, Robert, additional, Szomolay, Barbara, additional, Cossins, Benjamin C, additional, Rice, Christopher M., additional, Li, Jasmine, additional, Tyrrell, Victoria J, additional, McLeod, Louise, additional, Holmans, Peter, additional, O’Donnell, Valerie B, additional, Taylor, Philip R, additional, Turner, Stephen J., additional, Jenkins, Brendan J., additional, Jones, Gareth W, additional, Topley, Nicholas, additional, Williams, Nigel M, additional, and Jones, Simon A, additional

Published
2022
Full Text
View/download PDF

11. Th17-to-Tfh plasticity during periodontitis limits disease pathology

Author

McClure, Flora A., Wemyss, Kelly, Cox, Joshua R., Bridgeman, Hayley M., Prise, Ian E., King, James I., Jaigirdar, Shafqat, Whelan, Annie, Jones, Gareth W., Grainger, John R., Hepworth, Matthew R., and Konkel, Joanne E.

Abstract

Th17 cell plasticity is crucial for development of autoinflammatory disease pathology. Periodontitis is a prevalent inflammatory disease where Th17 cells mediate key pathological roles, yet whether they exhibit any functional plasticity remains unexplored. We found that during periodontitis, gingival IL-17 fate-mapped T cells still predominantly produce IL-17A, with little diversification of cytokine production. However, plasticity of IL-17 fate-mapped cells did occur during periodontitis, but in the gingiva draining lymph node. Here, some Th17 cells acquired features of Tfh cells, a functional plasticity that was dependent on IL-6. Notably, Th17-to-Tfh diversification was important to limit periodontitis pathology. Preventing Th17-to-Tfh plasticity resulted in elevated periodontal bone loss that was not simply due to increased proportions of conventional Th17 cells. Instead, loss of Th17-to-Tfh cells resulted in reduced IgG levels within the oral cavity and a failure to restrict the biomass of the oral commensal community. Thus, our data identify a novel protective function for a subset of otherwise pathogenic Th17 cells during periodontitis.

Published
2024
Full Text
View/download PDF

12. Tracking Cardiovascular Comorbidity in Models of Chronic Inflammatory Disease.

Author

Morrin AS, Eastham S, Williams AS, and Jones GW

Subjects
Animals, Mice, Comorbidity, Inflammation complications, Aorta, Thoracic, Arthritis, Experimental complications, Cardiovascular Diseases etiology
Abstract

Immune-mediated inflammatory diseases (IMIDs) are commonly associated with complex coexisting conditions, and cardiovascular comorbidities are a common cause of mortality in systemic inflammation. Experimental models of disease provide an opportunity to dissect inflammatory mechanisms that promote damage to vascular tissues affected by comorbidity. Here, we describe methods to recover the thoracic aorta from mice during experimental inflammatory arthritis and assess vascular constriction responses by isometric tension myography. To complement the assessment of functional changes in the vasculature during inflammatory arthritis, we also outline a method to characterize vascular inflammation by immunohistochemistry., (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2023
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results