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378 results on '"Ferris, Stephen P."'

3. Business acumen: What it means to logisticians

Author

O'Brien, Kristina M., LtCol and Ferris, Stephen P., CDR

Subjects
INDUSTRIAL PLANNING, MANAGEMENT IMPROVEMENT, LOGISTICS - Armed Forces - United States
Abstract

illus tab bibliog

Published
2009

4. CD5 expression by dendritic cells directs T cell immunity and sustains immunotherapy responses

Author

He, Mingyu, Roussak, Kate, Ma, Feiyang, Borcherding, Nicholas, Garin, Vince, White, Mike, Schutt, Charles, Jensen, Trine I, Zhao, Yun, Iberg, Courtney A, Shah, Kairav, Bhatia, Himanshi, Korenfeld, Daniel, Dinkel, Sabrina, Gray, Judah, Ulezko Antonova, Alina, Ferris, Stephen, Donermeyer, David, Lindestam Arlehamn, Cecilia, Gubin, Matthew M, Luo, Jingqin, Gorvel, Laurent, Pellegrini, Matteo, Sette, Alessandro, Tung, Thomas, Bak, Rasmus, Modlin, Robert L, Fields, Ryan C, Schreiber, Robert D, Allen, Paul M, and Klechevsky, Eynav

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Immunization, Immunotherapy, Vaccine Related, 5.1 Pharmaceuticals, Good Health and Well Being, Humans, CD8-Positive T-Lymphocytes, Cell Differentiation, Dendritic Cells, Melanoma, CD5 Antigens, Immune Checkpoint Inhibitors, T-Lymphocytes, Helper-Inducer, General Science & Technology
Abstract

The induction of proinflammatory T cells by dendritic cell (DC) subtypes is critical for antitumor responses and effective immune checkpoint blockade (ICB) therapy. Here, we show that human CD1c+CD5+ DCs are reduced in melanoma-affected lymph nodes, with CD5 expression on DCs correlating with patient survival. Activating CD5 on DCs enhanced T cell priming and improved survival after ICB therapy. CD5+ DC numbers increased during ICB therapy, and low interleukin-6 (IL-6) concentrations promoted their de novo differentiation. Mechanistically, CD5 expression by DCs was required to generate optimally protective CD5hi T helper and CD8+ T cells; further, deletion of CD5 from T cells dampened tumor elimination in response to ICB therapy in vivo. Thus, CD5+ DCs are an essential component of optimal ICB therapy.

Published
2023

6. Outsourcing the sinews of war: Contractor logistics

Author

Ferris, Stephen P., LCDR and Keithly, David M.

Subjects
INTEGRATED LOGISTIC SUPPORT, MANAGEMENT IMPROVEMENT, LOGISTICS - Army - United States, CONTRACTED SERVICES
Abstract

illus por bibliog

Published
2001

11. Crisis in strategic sealift

Author

Ferris, Stephen P., LT

Subjects
SEALIFT, MERCHANT MARINE - United States
Abstract

illus

Published
1996

23. Optimization of the Irf8+32-kb enhancer disrupts dendritic cell lineage segregation

Author

Ou, Feiya, Liu, Tian-Tian, Desai, Pritesh, Ferris, Stephen T., Kim, Sunkyung, Shen, Haolin, Ohara, Ray A., Jo, Suin, Chen, Jing, Postoak, J. Luke, Du, Siling, Diamond, Michael S., Murphy, Theresa L., and Murphy, Kenneth M.

Abstract

Autoactivation of lineage-determining transcription factors mediates bistable expression, generating distinct cell phenotypes essential for complex body plans. Classical type 1 dendritic cell (cDC1) and type 2 dendritic cell (cDC2) subsets provide nonredundant functions for defense against distinct immune challenges. Interferon regulatory factor 8 (IRF8), the cDC1 lineage-determining transcription factor, undergoes autoactivation in cDC1 progenitors to establish cDC1 identity, yet its expression is downregulated during cDC2 differentiation by an unknown mechanism. This study reveals that the Irf8+32-kb enhancer, responsible for IRF8 autoactivation, is naturally suboptimized with low-affinity IRF8 binding sites. Introducing multiple high-affinity IRF8 sites into the Irf8+32-kb enhancer causes a gain-of-function effect, leading to erroneous IRF8 autoactivation in specified cDC2 progenitors, redirecting them toward cDC1 and a novel hybrid DC subset with mixed-lineage phenotypes. Further, this also causes a loss-of-function effect, reducing Irf8expression in cDC1s. These developmental alterations critically impair both cDC1-dependent and cDC2-dependent arms of immunity. Collectively, our findings underscore the significance of enhancer suboptimization in the developmental segregation of cDCs required for normal immune function.

Published
2024
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30. Cultural, trust, and transparency effects on the use of anchoring in mergers and acquisitions.

Author

Ferris, Stephen P., Jayaraman, Narayanan, and Min-Yu Liao, (Stella)

Subjects
MERGERS & acquisitions, TRUST, ANCHORING effect, PRICES, RISK aversion
Abstract

Although price anchoring is a global phenomenon, we find that country cultures, trust levels, and information/legal transparency affect its use in determining target offer prices. Price anchoring is associated with cultures that deemphasize long-term orientation, uncertainty avoidance, and personal indulgence. Acquirers from countries with low levels of trust in people or the legal system are more likely to anchor their bids. Anchoring is more frequently observed in countries where information and legal transparency is poor. We find that the use of anchoring can result in reduced long-term performance by acquirers. [ABSTRACT FROM AUTHOR]

Published
2024
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44. Ablation of cDC2 development by triple mutations within the Zeb2enhancer

Author

Liu, Tian-Tian, Kim, Sunkyung, Desai, Pritesh, Kim, Do-Hyun, Huang, Xiao, Ferris, Stephen T., Wu, Renee, Ou, Feiya, Egawa, Takeshi, Van Dyken, Steven J., Diamond, Michael S., Johnson, Peter F., Kubo, Masato, Murphy, Theresa L., and Murphy, Kenneth M.

Abstract

The divergence of the common dendritic cell progenitor1–3(CDP) into the conventional type 1 and type 2 dendritic cell (cDC1 and cDC2, respectively) lineages4,5is poorly understood. Some transcription factors act in the commitment of already specified progenitors—such as BATF3, which stabilizes Irf8autoactivation at the +32 kb Irf8enhancer4,6—but the mechanisms controlling the initial divergence of CDPs remain unknown. Here we report the transcriptional basis of CDP divergence and describe the first requirements for pre-cDC2 specification. Genetic epistasis analysis7suggested that Nfil3acts upstream of Id2, Batf3and Zeb2in cDC1 development but did not reveal its mechanism or targets. Analysis of newly generated NFIL3 reporter mice showed extremely transient NFIL3 expression during cDC1 specification. CUT&RUN and chromatin immunoprecipitation followed by sequencing identified endogenous NFIL3 binding in the –165 kb Zeb2enhancer8at three sites that also bind the CCAAT-enhancer-binding proteins C/EBPα and C/EBPβ. In vivo mutational analysis using CRISPR–Cas9 targeting showed that these NFIL3–C/EBP sites are functionally redundant, with C/EBPs supporting and NFIL3 repressing Zeb2expression at these sites. A triple mutation of all three NFIL3–C/EBP sites ablated Zeb2expression in myeloid, but not lymphoid progenitors, causing the complete loss of pre-cDC2 specification and mature cDC2 development in vivo. These mice did not generate T helper 2 (TH2) cell responses against Heligmosomoides polygyrusinfection, consistent with cDC2 supporting TH2 responses to helminths9–11. Thus, CDP divergence into cDC1 or cDC2 is controlled by competition between NFIL3 and C/EBPs at the –165 kb Zeb2enhancer.

Published
2024
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