C
Cynthia J. Guidi
Researcher at University of Massachusetts Medical School
Publications - 9
Citations - 1065
Cynthia J. Guidi is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: Chromatin remodeling & Chromatin. The author has an hindex of 7, co-authored 9 publications receiving 989 citations. Previous affiliations of Cynthia J. Guidi include University of Virginia.
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Journal ArticleDOI
Lymph node–resident lymphatic endothelial cells mediate peripheral tolerance via Aire-independent direct antigen presentation
Jarish N. Cohen,Cynthia J. Guidi,Eric F. Tewalt,Hui Qiao,Sherin J. Rouhani,Alanna Ruddell,Andrew G. Farr,Kenneth S. K. Tung,Victor H. Engelhard +8 more
TL;DR: It is demonstrated that LN-resident lymphatic endothelial cells express multiple peripheral tissue antigens (PTAs) independent of the autoimmune regulator (Aire), and that other LN stromal subpopulations express distinct PTAs by mechanisms that vary in their Aire dependence.
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Disruption of Ini1 Leads to Peri-Implantation Lethality and Tumorigenesis in Mice
Cynthia J. Guidi,Arthur T. Sands,Brian Zambrowicz,Tod K. Turner,Delia A. Demers,William Webster,Thomas W. Smith,Anthony N. Imbalzano,Stephen N. Jones +8 more
TL;DR: Ini1 is essential for embryo viability and for repression of oncogenesis in the adult organism, and disruption of Ini1 expression in mice results in early embryonic lethality.
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Lymphatic endothelial cells induce tolerance via PD-L1 and lack of costimulation leading to high-level PD-1 expression on CD8 T cells.
Eric F. Tewalt,Jarish N. Cohen,Sherin J. Rouhani,Cynthia J. Guidi,Hui Qiao,Shawn P. Fahl,Mark R. Conaway,Timothy P. Bender,Kenneth S. K. Tung,Anthony T. Vella,Adam J. Adler,Lieping Chen,Victor H. Engelhard +12 more
TL;DR: It is shown that rescue of tyrosinase-specific T(CD8) by interference with PD-1 or provision of costimulation results in autoimmune vitiligo, demonstrating that LECs are significant, albeit suboptimal, antigen-presenting cells.
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Mammalian SWI-SNF Complexes Contribute to Activation of the hsp70 Gene
Ivana L. de la Serna,Kerri A. Carlson,David A. Hill,Cynthia J. Guidi,Ryan O. Stephenson,Saïd Sif,Robert E. Kingston,Anthony N. Imbalzano +7 more
TL;DR: It is proposed that the requirement for mammalian SWI-SNF complexes in gene activation events will be specific to individual genes and signaling pathways, and nonfunctional, dominant negative complexes may be formed.
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Transcriptional compensation for loss of an allele of the Ini1 tumor suppressor.
TL;DR: Calculated levels of Ini1 protein and message are roughly equivalent to the levels observed in wild type counterparts, which is the first report describing transcriptional compensation for haploinsufficiency of a tumor suppressor gene.