Kyle J. Lorentsen

551 total citations
7 papers, 317 citations indexed

About

Kyle J. Lorentsen is a scholar working on Immunology, Surgery and Genetics. According to data from OpenAlex, Kyle J. Lorentsen has authored 7 papers receiving a total of 317 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Immunology, 1 paper in Surgery and 1 paper in Genetics. Recurrent topics in Kyle J. Lorentsen's work include Immune Cell Function and Interaction (4 papers), IL-33, ST2, and ILC Pathways (3 papers) and Immunotherapy and Immune Responses (3 papers). Kyle J. Lorentsen is often cited by papers focused on Immune Cell Function and Interaction (4 papers), IL-33, ST2, and ILC Pathways (3 papers) and Immunotherapy and Immune Responses (3 papers). Kyle J. Lorentsen collaborates with scholars based in United States. Kyle J. Lorentsen's co-authors include Dorina Avram, Jonathan Cho, Mohammad Nizam Uddin, Danielle Califano, Qi Yang, Avinash Bhandoola, Hongmin Li, Theodore T. Drashansky, Maigan A. Brusko and Joshua M. Stewart and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Nature Communications and Immunity.

In The Last Decade

Kyle J. Lorentsen

7 papers receiving 315 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Kyle J. Lorentsen United States	7	257	83	75	35	22	7	317
Olav Sundnes Norway	11	192 0.7×	149 1.8×	30 0.4×	12 0.3×	26 1.2×	16	331
Mónica Romera‐Hernández Netherlands	8	220 0.9×	102 1.2×	65 0.9×	17 0.5×	70 3.2×	9	313
Laura Surace France	6	259 1.0×	59 0.7×	48 0.6×	20 0.6×	100 4.5×	10	348
Thibaut Perchet France	9	262 1.0×	134 1.6×	40 0.5×	13 0.4×	20 0.9×	12	316
Tom Franckson Germany	6	152 0.6×	55 0.7×	47 0.6×	20 0.6×	72 3.3×	7	282
Erika Hayes United States	7	275 1.1×	100 1.2×	40 0.5×	11 0.3×	45 2.0×	8	347
Satoshi Sugaya Japan	8	88 0.3×	97 1.2×	76 1.0×	88 2.5×	83 3.8×	15	305
V. Bruner Italy	7	95 0.4×	36 0.4×	72 1.0×	95 2.7×	22 1.0×	9	295
Vivien Holecska Germany	5	183 0.7×	38 0.5×	52 0.7×	8 0.2×	18 0.8×	5	222
Ryusuke Munemura Japan	7	113 0.4×	50 0.6×	65 0.9×	16 0.5×	67 3.0×	8	218

Countries citing papers authored by Kyle J. Lorentsen

Since Specialization

Citations

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

Fields of papers citing papers by Kyle J. Lorentsen

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Kyle J. Lorentsen. 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 Kyle J. Lorentsen. The network helps show where Kyle J. Lorentsen may publish in the future.

Co-authorship network of co-authors of Kyle J. Lorentsen

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

All Works

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7 of 7 papers shown

1.

Drashansky, Theodore T., Eric Y. Helm, Zhiguang Huo, et al.. (2019). Bcl11b prevents fatal autoimmunity by promoting T _reg cell program and constraining innate lineages in T _reg cells. Science Advances. 5(8). eaaw0480–eaaw0480. 20 indexed citations

2.

Lorentsen, Kyle J., Jonathan Cho, Xiaoping Luo, et al.. (2018). Bcl11b is essential for licensing Th2 differentiation during helminth infection and allergic asthma. Nature Communications. 9(1). 1679–1679. 26 indexed citations

3.

Bryant, Andrew J., Vinayak Shenoy, Chunhua Fu, et al.. (2017). Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension. American Journal of Respiratory Cell and Molecular Biology. 58(2). 170–180. 33 indexed citations

4.

Cho, Jonathan, Joshua M. Stewart, Theodore T. Drashansky, et al.. (2017). An antigen-specific semi-therapeutic treatment with local delivery of tolerogenic factors through a dual-sized microparticle system blocks experimental autoimmune encephalomyelitis. Biomaterials. 143. 79–92. 71 indexed citations

5.

Abboud, Georges, Vikas Tahiliani, Pritesh Desai, et al.. (2016). Transcription Factor Bcl11b Controls Effector and Memory CD8 T cell Fate Decision and Function during Poxvirus Infection. Frontiers in Immunology. 7. 425–425. 15 indexed citations

6.

Uddin, Mohammad Nizam, Kyle J. Lorentsen, Jonathan Cho, et al.. (2016). Transcription factor Bcl11b sustains iNKT1 and iNKT2 cell programs, restricts iNKT17 cell program, and governs iNKT cell survival. Proceedings of the National Academy of Sciences. 113(27). 7608–7613. 19 indexed citations

7.

Califano, Danielle, Jonathan Cho, Mohammad Nizam Uddin, et al.. (2015). Transcription Factor Bcl11b Controls Identity and Function of Mature Type 2 Innate Lymphoid Cells. Immunity. 43(2). 354–368. 133 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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