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Articles by Daniel Chauss
Role of local complement activation in kidney fibrosis and repair
Review Series Open Access | 10.1172/JCI188345 Published in Volume 135, Issue 12 on June 16, 2025 J Clin Invest. 2025;135(12):e188345. https://doi.org/10.1172/JCI188345. © 2025 Portilla et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
A PI3Kδ-Foxo1-FasL signaling amplification loop rewires CD4+ T helper cell signaling, differentiation and epigenetic remodeling
Abstract While inputs regulating CD4+ T helper cell (Th) differentiation are well-defined, the integration of downstream signaling with transcriptional and epigenetic programs that define Th-lineage identity remain unresolved. PI3K signaling is a critical regulator of T cell function; activating mutations affecting PI3Kδ result in an immunodeficiency with multiple T cell defects.
Host-virus chimeric events in SARS-CoV2 infected cells are infrequent and artifactual
Virus-Cell Interactions Bingyu Yan, Srishti Chakravorty, Carmen Mirabelli, Luopin Wang, Jorge L. Trujillo-Ochoa, Daniel Chauss, Dhaneshwar Kumar, Michail S. Lionakis, Matthew R Olson, Christiane E. Wobus, Behdad Afzali, Majid Kazemian DOI: 10.1128/JVI.00294-21 ABSTRACT Pathogenic mechanisms underlying severe SARS-CoV2 infection remain largely unelucidated.
SARS-CoV-2 drives JAK1/2-dependent local complement hyperactivation
Abstract Patients with coronavirus disease 2019 (COVID-19) present a wide range of acute clinical manifestations affecting the lungs, liver, kidneys and gut. Angiotensin converting enzyme (ACE) 2, the best-characterized entry receptor for the disease-causing virus SARS-CoV-2, is highly expressed in the aforementioned tissues. However, the pathways that underlie the disease are still poorly understood.
An autocrine Vitamin D-driven Th1 shutdown program can be exploited for COVID-19
New Results View ORCID ProfileReuben McGregor, View ORCID ProfileDaniel Chauss, View ORCID ProfileTilo Freiwald, View ORCID ProfileBingyu Yan, View ORCID ProfileLuopin Wang, View ORCID ProfileEstefania Nova-Lamperti, Zonghao Zhang, Heather Teague, Erin E West, View ORCID ProfileJack Bibby, Audrey Kelly, Amna Malik, Alexandra F Freeman, View ORCID ProfileDaniella Schwartz, Didier Portilla, View ORCID ProfileSusan John, Paul Lavender, View ORCID ProfileMichail S Lionakis, View ORCID...
Diapedesis-Induced Integrin Signaling via LFA-1 Facilitates Tissue Immunity by Inducing Intrinsic Complement C3 Expression in Immune Cells
Highlights • Diapedesis induces C3 expression as a feature of immune cells in tissue • C3 transcription is LFA-1 dependent and integral to normal immune cell activity • Defective C3 expression underlies human primary immune deficiency disease LAD-1 • The integrin network is a key driver of complosome activity and cell function Summary Intrinsic complement C3 activity is integral to human T helper type 1 (Th1) and cytotoxic T cell responses.
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