John R. Šedý

4.6k total citations · 2 hit papers
28 papers, 3.6k citations indexed

About

John R. Šedý is a scholar working on Immunology, Epidemiology and Oncology. According to data from OpenAlex, John R. Šedý has authored 28 papers receiving a total of 3.6k indexed citations (citations by other indexed papers that have themselves been cited), including 25 papers in Immunology, 8 papers in Epidemiology and 7 papers in Oncology. Recurrent topics in John R. Šedý's work include Immune Cell Function and Interaction (23 papers), T-cell and B-cell Immunology (18 papers) and Cytomegalovirus and herpesvirus research (8 papers). John R. Šedý is often cited by papers focused on Immune Cell Function and Interaction (23 papers), T-cell and B-cell Immunology (18 papers) and Cytomegalovirus and herpesvirus research (8 papers). John R. Šedý collaborates with scholars based in United States, Slovakia and Egypt. John R. Šedý's co-authors include Kenneth M. Murphy, Carl F. Ware, Jianfei Yang, Michelle A. Hurchla, Theresa L. Murphy, Maya Gavrieli, Theresa L. Murphy, Soo Young Yang, Nezih Cereb and Maryam Afkarian and has published in prestigious journals such as Journal of Biological Chemistry, Immunity and Nature reviews. Immunology.

In The Last Decade

John R. Šedý

28 papers receiving 3.6k citations

Hit Papers

T-bet is a STAT1-induced regulator of IL-12R expression i... 2002 2026 2010 2018 2002 2003 250 500 750

Peers

John R. Šedý
Stanley Adoro United States
Terry I. Guinter United States
Youjin Lee United States
Cory L. Ahonen United States
Patrick Schaerli Switzerland
Matthew A. Burchill United States
Laura Bover United States
Maya Gavrieli United States
John R. Šedý
Citations per year, relative to John R. Šedý John R. Šedý (= 1×) peers Satoru Kumaki

Countries citing papers authored by John R. Šedý

Since Specialization
Citations

This map shows the geographic impact of John R. Šedý'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 John R. Šedý with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites John R. Šedý more than expected).

Fields of papers citing papers by John R. Šedý

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John R. Šedý. 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 John R. Šedý. The network helps show where John R. Šedý may publish in the future.

Co-authorship network of co-authors of John R. Šedý

This figure shows the co-authorship network connecting the top 25 collaborators of John R. Šedý. A scholar is included among the top collaborators of John R. Šedý 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 John R. Šedý. John R. Šedý is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Virgen‐Slane, Richard, Lisa Elmeń, Marisol Veny, et al.. (2022). Btla signaling in conventional and regulatory lymphocytes coordinately tempers humoral immunity in the intestinal mucosa. Cell Reports. 38(12). 110553–110553. 12 indexed citations
2.
Veny, Marisol, Karolı́na Kuchárová, Wai Lin, et al.. (2020). Contactin-1 Is Required for Peripheral Innervation and Immune Homeostasis Within the Intestinal Mucosa. Frontiers in Immunology. 11. 1268–1268. 10 indexed citations
3.
Šedý, John R. & Parham Ramezani-Rad. (2019). HVEM network signaling in cancer. Advances in cancer research. 142. 145–186. 39 indexed citations
4.
Ward-Kavanagh, Lindsay K., Wai Lin, John R. Šedý, & Carl F. Ware. (2016). The TNF Receptor Superfamily in Co-stimulating and Co-inhibitory Responses. Immunity. 44(5). 1005–1019. 320 indexed citations
5.
Šedý, John R., et al.. (2016). Targeting the HVEM-BTLA-CD160-LIGHT network in Psoriasis. The Journal of Immunology. 196(1_Supplement). 124.42–124.42. 1 indexed citations
6.
Šedý, John R., Vasileios Bekiaris, & Carl F. Ware. (2014). Tumor Necrosis Factor Superfamily in Innate Immunity and Inflammation. Cold Spring Harbor Perspectives in Biology. 7(4). a016279–a016279. 78 indexed citations
7.
Bekiaris, Vasileios, et al.. (2013). The Inhibitory Receptor BTLA Controls γδ T Cell Homeostasis and Inflammatory Responses. Immunity. 39(6). 1082–1094. 76 indexed citations
8.
Ware, Carl F. & John R. Šedý. (2011). TNF Superfamily Networks: bidirectional and interference pathways of the herpesvirus entry mediator (TNFSF14). Current Opinion in Immunology. 23(5). 627–631. 86 indexed citations
9.
Šedý, John R., Patricia G. Spear, & Carl F. Ware. (2008). Cross-regulation between herpesviruses and the TNF superfamily members. Nature reviews. Immunology. 8(11). 861–873. 64 indexed citations
10.
Ong, Chin‐Tong, John R. Šedý, Kenneth M. Murphy, & Raphael Kopan. (2008). Notch and Presenilin Regulate Cellular Expansion and Cytokine Secretion but Cannot Instruct Th1/Th2 Fate Acquisition. PLoS ONE. 3(7). e2823–e2823. 77 indexed citations
11.
Wilker, Peter R., John R. Šedý, Vadim Grigura, Theresa L. Murphy, & Kenneth M. Murphy. (2007). Evidence for carbohydrate recognition and homotypic and heterotypic binding by the TIM family. International Immunology. 19(6). 763–773. 40 indexed citations
12.
Gavrieli, Maya, John R. Šedý, Christopher A. Nelson, & Kenneth M. Murphy. (2006). BTLA and HVEM Cross Talk Regulates Inhibition and Costimulation. Advances in immunology. 92. 157–185. 41 indexed citations
13.
Murphy, Kenneth M., Christopher A. Nelson, & John R. Šedý. (2006). Balancing co-stimulation and inhibition with BTLA and HVEM. Nature reviews. Immunology. 6(9). 671–681. 254 indexed citations
14.
Hurchla, Michelle A., et al.. (2005). B and T Lymphocyte Attenuator Exhibits Structural and Expression Polymorphisms and Is Highly Induced in Anergic CD4+ T Cells. The Journal of Immunology. 174(6). 3377–3385. 150 indexed citations
15.
Hurchla, Michelle A., et al.. (2005). B and T lymphocyte attenuator exhibits structural and expression polymorphisms and is highly induced in anergic CD4+ T cells. The Journal of Immunology. 174(9). 5884a–5884. 8 indexed citations
16.
Šedý, John R., Maya Gavrieli, Karen G. Potter, et al.. (2004). B and T lymphocyte attenuator regulates T cell activation through interaction with herpesvirus entry mediator. Nature Immunology. 6(1). 90–98. 499 indexed citations
17.
Yassai, Maryam, John R. Šedý, Tara D. Wehrly, et al.. (2003). T cell receptor CDR3 loop length repertoire is determined primarily by features of the V(D)J recombination reaction. European Journal of Immunology. 33(6). 1568–1575. 35 indexed citations
18.
Watanabe, Norihiko, Maya Gavrieli, John R. Šedý, et al.. (2003). BTLA is a lymphocyte inhibitory receptor with similarities to CTLA-4 and PD-1. Nature Immunology. 4(7). 670–679. 695 indexed citations breakdown →
19.
Afkarian, Maryam, John R. Šedý, Jianfei Yang, et al.. (2002). T-bet is a STAT1-induced regulator of IL-12R expression in naïve CD4+ T cells. Nature Immunology. 3(6). 549–557. 803 indexed citations breakdown →
20.
Sperling, Anne I., John R. Šedý, N. Manjunath, et al.. (1998). Cutting Edge: TCR Signaling Induces Selective Exclusion of CD43 from the T Cell-Antigen-Presenting Cell Contact Site. The Journal of Immunology. 161(12). 6459–6462. 108 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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