Nathan Karin
About
Nathan Karin is a scholar working on Immunology, Oncology and Molecular Biology.
According to data from OpenAlex, Nathan Karin has authored 62 papers receiving a total of 5.2k indexed citations (citations by other indexed papers that have themselves been cited), including 58 papers in Immunology, 30 papers in Oncology and 8 papers in Molecular Biology. Recurrent topics in Nathan Karin's work include Immunotherapy and Immune Responses (37 papers), T-cell and B-cell Immunology (34 papers) and Chemokine receptors and signaling (23 papers). Nathan Karin is often cited by papers focused on Immunotherapy and Immune Responses (37 papers), T-cell and B-cell Immunology (34 papers) and Chemokine receptors and signaling (23 papers). Nathan Karin collaborates with scholars based in Israel, United States and Germany. Nathan Karin's co-authors include Gizi Wildbaum, Lawrence Steinman, Francisco Sánchez‐Madrid, Lawrence C. Fritz, Ted Yednock, Catherine Cannon, Hila Razon, Sawsan Youssef, Nikolaus C. Netzer and Yaniv Zohar and has published in prestigious journals such as Nature, Science and Proceedings of the National Academy of Sciences.
In The Last Decade
Nathan Karin
62 papers receiving 5.1k citations
Hit Papers
Peers — A (Enhanced Table)
Peers by citation overlap · career bar shows stage (early→late) cites · hero ref
| Name | h | Career | Trend | Papers | Cites | |||||
|---|---|---|---|---|---|---|---|---|---|---|
| Nathan Karin Israel | 35 | 3.3k | 1.7k | 1.0k | 794 | 600 | 62 | 5.2k | ||
| Shixin Qin United States | 37 | 6.4k 1.9× | 2.9k 1.7× | 1.2k 1.2× | 462 0.6× | 721 1.2× | 49 | 9.1k | ||
| David Chantry United States | 35 | 3.0k 0.9× | 1.8k 1.1× | 1.1k 1.1× | 290 0.4× | 636 1.1× | 74 | 5.5k | ||
| Thomas Hünig Germany | 41 | 4.3k 1.3× | 1.1k 0.6× | 1.1k 1.1× | 309 0.4× | 229 0.4× | 137 | 5.9k | ||
| José Carlos Gutierrez‐Ramos United States | 34 | 4.5k 1.3× | 2.0k 1.2× | 1.6k 1.6× | 242 0.3× | 1.3k 2.2× | 55 | 7.9k | ||
| Norman Boiani United States | 14 | 2.2k 0.7× | 1.4k 0.8× | 1.5k 1.5× | 284 0.4× | 636 1.1× | 14 | 4.7k | ||
| Carol L. Vanderlugt United States | 23 | 2.6k 0.8× | 558 0.3× | 537 0.5× | 800 1.0× | 176 0.3× | 26 | 3.7k | ||
| Cédric Auffray France | 25 | 4.1k 1.2× | 879 0.5× | 1.3k 1.3× | 215 0.3× | 289 0.5× | 40 | 5.8k | ||
| Laurence Boumsell France | 48 | 3.4k 1.0× | 886 0.5× | 1.3k 1.3× | 1.0k 1.3× | 482 0.8× | 152 | 6.8k | ||
| Miyuki Nishimura Japan | 20 | 2.9k 0.9× | 2.3k 1.3× | 935 0.9× | 158 0.2× | 536 0.9× | 27 | 4.7k | ||
| Uta E. Höpken Germany | 34 | 3.0k 0.9× | 1.4k 0.8× | 953 1.0× | 305 0.4× | 211 0.4× | 79 | 4.4k |
Countries citing papers authored by Nathan Karin
Since
Specialization
Citations
This map shows the geographic impact of Nathan Karin'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 Nathan Karin with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Nathan Karin more than expected).
Fields of papers citing papers by Nathan Karin
Since
Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences
This network shows the impact of papers produced by Nathan Karin. 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 Nathan Karin. The network helps show where Nathan Karin may publish in the future.
Co-authorship network of co-authors of Nathan Karin
This figure shows the co-authorship network connecting the top 25 collaborators of Nathan Karin. A scholar is included among the top collaborators of Nathan Karin 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 Nathan Karin. Nathan Karin is excluded from the visualization to improve readability, since they are connected to all nodes in the network.
All Works
1.
Blattner, C, Viktor Fleming, Rebekka Weber, et al.. (2018). CCR5+ Myeloid-Derived Suppressor Cells Are Enriched and Activated in Melanoma Lesions. Cancer Research. 78(1). 157–167.
2.
Harris, Nicholas, Juraj Koppel, Ferenc Zsila, et al.. (2016). Mechanism of action and efficacy of RX-111, a thieno[2,3-c]pyridine derivative and small molecule inhibitor of protein interaction with glycosaminoglycans (SMIGs), in delayed-type hypersensitivity, TNBS-induced colitis and experimental autoimmune encephalomyelitis. Inflammation Research. 65(4). 285–294.
3.
Karin, Nathan & Gizi Wildbaum. (2015). The role of chemokines in adjusting the balance between CD4+ effector T cell subsets and FOXp3-negative regulatory T cells. International Immunopharmacology. 28(2). 829–835.
4.
Izhak, Liat, Gizi Wildbaum, Steffen Jung, et al.. (2012). Dissecting the Autocrine and Paracrine Roles of the CCR2-CCL2 Axis in Tumor Survival and Angiogenesis. PLoS ONE. 7(1). e28305–e28305.
5.
Wildbaum, Gizi, Yaniv Zohar, & Nathan Karin. (2010). Antigen-Specific CD25−Foxp3−IFN-γhighCD4+ T Cells Restrain the Development of Experimental Allergic Encephalomyelitis by Suppressing Th17. American Journal Of Pathology. 176(6). 2764–2775.
6.
Izhak, Liat, Gizi Wildbaum, Uri Weinberg, et al.. (2009). Predominant Expression of CCL2 at the Tumor Site of Prostate Cancer Patients Directs a Selective Loss of Immunological Tolerance to CCL2 That Could Be Amplified in a Beneficial Manner. The Journal of Immunology. 184(2). 1092–1101.
7.
Izhak, Liat, Gizi Wildbaum, Yaniv Zohar, et al.. (2009). A Novel Recombinant Fusion Protein Encoding a 20-Amino Acid Residue of the Third Extracellular (E3) Domain of CCR2 Neutralizes the Biological Activity of CCL2. The Journal of Immunology. 183(1). 732–739.
8.
Zohar, Yaniv, et al.. (2008). CXCL12 (SDF-1α) suppresses ongoing experimental autoimmune encephalomyelitis by selecting antigen-specific regulatory T cells. The Journal of Experimental Medicine. 205(11). 2643–2655.
9.
Lugassy, Jennie, John A. McGrath, Peter Itin, et al.. (2007). KRT14 Haploinsufficiency Results in Increased Susceptibility of Keratinocytes to TNF-α-Induced Apoptosis and Causes Naegeli–Franceschetti–Jadassohn Syndrome. Journal of Investigative Dermatology. 128(6). 1517–1524.
10.
Schif‐Zuck, Sagie, Gizi Wildbaum, & Nathan Karin. (2006). Coadministration of Plasmid DNA Constructs Encoding an Encephalitogenic Determinant and IL-10 Elicits Regulatory T Cell-Mediated Protective Immunity in the Central Nervous System. The Journal of Immunology. 177(11). 8241–8247.
11.
Schif‐Zuck, Sagie, Juergen Westermann, Nikolaus C. Netzer, et al.. (2005). Targeted Overexpression of IL-18 Binding Protein at the Central Nervous System Overrides Flexibility in Functional Polarization of Antigen-Specific Th2 Cells. The Journal of Immunology. 174(7). 4307–4315.
12.
Westermann, Jürgen, Ulrike Bode, Nathan Karin, et al.. (2005). Naive, Effector, and Memory T Lymphocytes Efficiently Scan Dendritic Cells In Vivo: Contact Frequency in T Cell Zones of Secondary Lymphoid Organs Does Not Depend on LFA-1 Expression and Facilitates Survival of Effector T Cells. The Journal of Immunology. 174(5). 2517–2524.
13.
Wildbaum, Gizi, et al.. (2004). Suppression of Ongoing Adjuvant-Induced Arthritis by Neutralizing the Function of the p28 Subunit of IL-27. The Journal of Immunology. 173(2). 1171–1178.
14.
Zohar, Yaniv, et al.. (2004). Suppression of Ongoing Experimental Autoimmune Encephalomyelitis by Neutralizing the Function of the p28 Subunit of IL-27. The Journal of Immunology. 173(10). 6465–6471.
15.
Wildbaum, Gizi, M Nahir, & Nathan Karin. (2003). Beneficial Autoimmunity to Proinflammatory Mediators Restrains the Consequences of Self-Destructive Immunity. Immunity. 19(5). 679–688.
16.
Wildbaum, Gizi, Nikolaus C. Netzer, & Nathan Karin. (2002). Tr1 cell–dependent active tolerance blunts the pathogenic effects of determinant spreading. Journal of Clinical Investigation. 110(5). 701–710.
17.
Netzer, Nikolaus C., et al.. (2002). Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis. The Journal of Immunology. 169(5). 2685–2693.
18.
Wildbaum, Gizi, Nikolaus C. Netzer, & Nathan Karin. (2002). Plasmid DNA Encoding IFN-γ-Inducible Protein 10 Redirects Antigen-Specific T Cell Polarization and Suppresses Experimental Autoimmune Encephalomyelitis. The Journal of Immunology. 168(11). 5885–5892.
19.
Wildbaum, Gizi, Sawsan Youssef, & Nathan Karin. (2000). A Targeted DNA Vaccine Augments the Natural Immune Response to Self TNF-α and Suppresses Ongoing Adjuvant Arthritis. The Journal of Immunology. 165(10). 5860–5866.
20.
Brocke, Stefan, Koenraad Gijbels, Mark Allegretta, et al.. (1996). Treatment of experimental encephalomyelitis with a peptide analogue of myelin basic protein. Nature. 379(6563). 343–346.
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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