His primary areas of investigation include Cell biology, T cell, Immunology, IL-2 receptor and Cytokine. The study incorporates disciplines such as Clonal anergy, Cellular differentiation, CD8, Histone and Epigenetics in addition to Cell biology. Andrew D. Wells studies CD28 which is a part of T cell.
Andrew D. Wells combines subjects such as Cell and In vivo with his study of Immunology. His IL-2 receptor research is classified as research in Cytotoxic T cell. His studies deal with areas such as Peripheral tolerance and Transplantation as well as Cytokine.
Andrew D. Wells spends much of his time researching Cell biology, T cell, Gene, Immunology and Genome-wide association study. His Cell biology research incorporates elements of IL-2 receptor, Cytokine, Cell division, Histone and FOXP3. The concepts of his T cell study are interwoven with issues in Cytotoxic T cell, Cancer research and Cyclin-dependent kinase.
He has included themes like Molecular biology and CD8 in his Cytotoxic T cell study. Many of his research projects under Gene are closely connected to Gene mapping with Gene mapping, tying the diverse disciplines of science together. His Immunology research includes elements of Apoptosis and Transplantation.
Gene, Computational biology, Genome-wide association study, Chromatin and Epigenetics are his primary areas of study. His study in the fields of Genome, Genome editing and Promoter under the domain of Gene overlaps with other disciplines such as Gene mapping. His Chromatin research is multidisciplinary, relying on both Mutation, Enhancer, Transcription factor, Epigenomics and Cell biology.
Andrew D. Wells has researched Cell biology in several fields, including RUNX2 and ALPL. His research in Epigenetics intersects with topics in Lymphatic system, Immunology, Lymphocyte and Cytotoxic T cell, Cytolysis. His T cell study contributes to a more complete understanding of Immune system.
The scientist’s investigation covers issues in Gene, Computational biology, Epigenetics, Genome-wide association study and Chromatin. His Computational biology research incorporates elements of Promoter, Gene expression, Regulation of gene expression and Cell. Andrew D. Wells combines subjects such as H3K4me3, Histone and Genetic variation with his study of Regulation of gene expression.
His work in Epigenetics addresses issues such as Immunology, which are connected to fields such as Cytolysis. The concepts of his Genome-wide association study study are interwoven with issues in Liver disease, Cancer, Disease and Effector. His Chromatin study incorporates themes from Enhancer, Transcription factor and Cell biology.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Blocking both signal 1 and signal 2 of T-cell activation prevents apoptosis of alloreactive T cells and induction of peripheral allograft tolerance
Yongsheng Li;Xian Chang Li;Xin Xiao Zheng;Andrew D. Wells.
Nature Medicine (1999)
Deacetylase inhibition promotes the generation and function of regulatory T cells
Ran Tao;Edwin F de Zoeten;Engin Özkaynak;Chunxia Chen.
Nature Medicine (2007)
Following the fate of individual T cells throughout activation and clonal expansion. Signals from T cell receptor and CD28 differentially regulate the induction and duration of a proliferative response.
Andrew D. Wells;Hrefna Gudmundsdottir;Laurence A. Turka.
Journal of Clinical Investigation (1997)
Requirement for T-cell apoptosis in the induction of peripheral transplantation tolerance.
Andrew D. Wells;Xian Chang Li;Yongsheng Li;Matthew C. Walsh.
Nature Medicine (1999)
Quantifying the frequency of alloreactive T cells in vivo: new answers to an old question.
Elliot J. Suchin;Peter B. Langmuir;Ed Palmer;Mohamed H. Sayegh.
Journal of Immunology (2001)
Recruitment of Foxp3+ T regulatory cells mediating allograft tolerance depends on the CCR4 chemokine receptor
Iris Lee;Liqing Wang;Andrew D. Wells;Martin E. Dorf.
Journal of Experimental Medicine (2005)
Dynamics and Requirements of T Cell Clonal Expansion In Vivo at the Single-Cell Level: Effector Function Is Linked to Proliferative Capacity
Hrefna Gudmundsdottir;Andrew D. Wells;Laurence A. Turka.
Journal of Immunology (1999)
Notch Signaling Augments T Cell Responsiveness by Enhancing CD25 Expression
Scott H. Adler;Elise Chiffoleau;Lanwei Xu;Nicole M. Dalton.
Journal of Immunology (2003)
Foxp3 and Toll-like receptor signaling balance Treg cell anabolic metabolism for suppression.
Valerie A Gerriets;Rigel J Kishton;Marc O Johnson;Marc O Johnson;Sivan Cohen.
Nature Immunology (2016)
The complement inhibitory protein DAF (CD55) suppresses T cell immunity in vivo.
Jianuo Liu;Takashi Miwa;Brendan Hilliard;Youhai Chen.
Journal of Experimental Medicine (2005)
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