Tim J. Vyse

2.9k total citations
17 papers, 567 citations indexed

About

Tim J. Vyse is a scholar working on Immunology, Rheumatology and Molecular Biology. According to data from OpenAlex, Tim J. Vyse has authored 17 papers receiving a total of 567 indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Immunology, 9 papers in Rheumatology and 5 papers in Molecular Biology. Recurrent topics in Tim J. Vyse's work include Systemic Lupus Erythematosus Research (9 papers), T-cell and B-cell Immunology (8 papers) and Immune Cell Function and Interaction (3 papers). Tim J. Vyse is often cited by papers focused on Systemic Lupus Erythematosus Research (9 papers), T-cell and B-cell Immunology (8 papers) and Immune Cell Function and Interaction (3 papers). Tim J. Vyse collaborates with scholars based in United Kingdom, United States and Austria. Tim J. Vyse's co-authors include Jerry S. Lanchbury, Philip L. De Jager, Angela M. Richardson, Alexander Gutin, Harinder Manku, John D. Rioux, Susanne Wagner, Kirsten M. Timms, Deborah S. Cunninghame Graham and Julia Reid and has published in prestigious journals such as International Journal of Molecular Sciences, Journal of the American Society of Nephrology and Human Molecular Genetics.

In The Last Decade

Tim J. Vyse

16 papers receiving 552 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Tim J. Vyse United Kingdom 11 350 248 138 88 81 17 567
Erica Moore United States 9 399 1.1× 184 0.7× 185 1.3× 47 0.5× 41 0.5× 13 583
Xana Kim-Howard United States 11 425 1.2× 335 1.4× 102 0.7× 69 0.8× 143 1.8× 16 672
Philip Tombleson United Kingdom 3 360 1.0× 336 1.4× 154 1.1× 76 0.9× 182 2.2× 3 639
Kevin Maas United States 13 152 0.4× 156 0.6× 146 1.1× 79 0.9× 52 0.6× 16 477
Nadia Alhashmi Oman 9 281 0.8× 233 0.9× 247 1.8× 59 0.7× 214 2.6× 15 678
Sylke Kaltenhäuser Germany 10 229 0.7× 269 1.1× 87 0.6× 50 0.6× 50 0.6× 13 499
K L Moser United States 12 426 1.2× 371 1.5× 159 1.2× 60 0.7× 106 1.3× 19 699
Fathiya Al-Murshedi Oman 10 266 0.8× 154 0.6× 221 1.6× 27 0.3× 99 1.2× 20 534
Š Rùzicková Czechia 11 203 0.6× 110 0.4× 168 1.2× 61 0.7× 59 0.7× 20 463
Geneviève Enault France 8 222 0.6× 121 0.5× 65 0.5× 52 0.6× 29 0.4× 10 397

Countries citing papers authored by Tim J. Vyse

Since Specialization
Citations

This map shows the geographic impact of Tim J. Vyse's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Tim J. Vyse with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Tim J. Vyse more than expected).

Fields of papers citing papers by Tim J. Vyse

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Tim J. Vyse. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Tim J. Vyse. The network helps show where Tim J. Vyse may publish in the future.

Co-authorship network of co-authors of Tim J. Vyse

This figure shows the co-authorship network connecting the top 25 collaborators of Tim J. Vyse. A scholar is included among the top collaborators of Tim J. Vyse based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Tim J. Vyse. Tim J. Vyse is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

17 of 17 papers shown
1.
Ferreira, Ricardo C., Xaquín Castro Dopico, Daniel B. Rainbow, et al.. (2019). Chronic Immune Activation in Systemic Lupus Erythematosus and the Autoimmune PTPN22 Trp620 Risk Allele Drive the Expansion of FOXP3+ Regulatory T Cells and PD-1 Expression. Frontiers in Immunology. 10. 2606–2606. 27 indexed citations
2.
Rainbow, Daniel B., Christopher L. Pinder, Clarke Pamela, et al.. (2018). The plasma biomarker soluble SIGLEC-1 is associated with the type I interferon transcriptional signature, ethnic background and renal disease in systemic lupus erythematosus. Arthritis Research & Therapy. 20(1). 152–152. 46 indexed citations
3.
Ferreira, Ricardo C., Whitney S. Thompson, Daniel B. Rainbow, et al.. (2017). Cells with Treg-specific FOXP3 demethylation but low CD25 are prevalent in autoimmunity. Journal of Autoimmunity. 84. 75–86. 64 indexed citations
4.
Fürnrohr, Barbara G., et al.. (2015). Osteoclast Differentiation Is Impaired in a Subgroup of SLE Patients and Correlates Inversely with Mycophenolate Mofetil Treatment. International Journal of Molecular Sciences. 16(8). 18825–18835. 9 indexed citations
5.
Armstrong, Don, Raphael Zidovetzki, Marta E. Alarcón‐Riquelme, et al.. (2014). GWAS identifies novel SLE susceptibility genes and explains the association of the HLA region. Genes and Immunity. 15(6). 347–354. 88 indexed citations
6.
Li, Ru, Caixia Li, Tanqi Lou, et al.. (2009). TRAC Variants Associate with IgA Nephropathy. Journal of the American Society of Nephrology. 20(6). 1359–1367. 5 indexed citations
7.
Rhodes, Benjamin, David Morris, Lakshman Subrahmanyan, et al.. (2008). Fine-mapping the genetic basis of CRP regulation in African Americans: a Bayesian approach. Human Genetics. 123(6). 633–642. 10 indexed citations
8.
Rhodes, Benjamin, et al.. (2008). Genetic determinants of basal C-reactive protein expression in Filipino systemic lupus erythematosus families. Genes and Immunity. 9(2). 153–160. 14 indexed citations
9.
Hepburn, A. L., Irvin A. Lampert, Donna Horncastle, et al.. (2007). In vivo evidence for apoptosis in the bone marrow in systemic lupus erythematosus. Annals of the Rheumatic Diseases. 66(8). 1106–1109. 42 indexed citations
10.
Hellquist, Anna, Katja Kivinen, Ulpu Saarialho‐Kere, et al.. (2007). The human GIMAP5 gene has a common polyadenylation polymorphism increasing risk to systemic lupus erythematosus. Journal of Medical Genetics. 44(5). 314–321. 64 indexed citations
11.
Graham, Deborah S. Cunninghame, Harinder Manku, Susanne Wagner, et al.. (2006). Association of IRF5 in UK SLE families identifies a variant involved in polyadenylation. Human Molecular Genetics. 16(6). 579–591. 100 indexed citations
12.
Jager, Philip L. De, Angela M. Richardson, Tim J. Vyse, & John D. Rioux. (2006). Genetic variation in toll‐like receptor 9 and susceptibility to systemic lupus erythematosus. Arthritis & Rheumatism. 54(4). 1279–1282. 50 indexed citations
13.
Russell, Ann, Tim J. Vyse, Derek L. Mattey, et al.. (2006). 23. CD3Z POLYMORPHISM IS ASSOCIATED WITH REDUCED EXPRESSION OF THE TCRCHAIN: ENRICHMENT IN PATIENTS WITH SEVERE RHEUMATOID ARTHRITIS.
14.
Rigby, Robert J., Michelle M. A. Fernando, & Tim J. Vyse. (2006). Mice, humans and haplotypes—the hunt for disease genes in SLE. Lara D. Veeken. 45(9). 1062–1067. 7 indexed citations
15.
Vyse, Tim J.. (2000). Complement factor H deficiency and atypical HUS. Arthritis Research & Therapy. 2(1). 1 indexed citations
16.
Vyse, Tim J., Linda Luxon, & Mark Walport. (1994). Audiovestibular manifestations of the antiphospholipid syndrome. The Journal of Laryngology & Otology. 108(1). 57–59. 28 indexed citations
17.
Sewry, C., Angela Clerk, J Z Heckmatt, et al.. (1991). Dystrophin abnormalities in polymyositis and dermatomyositis. Neuromuscular Disorders. 1(5). 333–339. 12 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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