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4. Urine Proteomics and Renal Single‐Cell Transcriptomics Implicate Interleukin‐16 in Lupus Nephritis

Author

Fava, Andrea, Rao, Deepak A, Mohan, Chandra, Zhang, Ting, Rosenberg, Avi, Fenaroli, Paride, Belmont, H Michael, Izmirly, Peter, Clancy, Robert, Trujillo, Jose Monroy, Fine, Derek, Arazi, Arnon, Berthier, Celine C, Davidson, Anne, James, Judith A, Diamond, Betty, Hacohen, Nir, Wofsy, David, Raychaudhuri, Soumya, Apruzzese, William, Network, the Accelerating Medicines Partnership in Rheumatoid Arthritis and Systemic Lupus Erythematosus, Buyon, Jill, and Petri, Michelle

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Kidney Disease, Clinical Research, Lupus, Autoimmune Disease, Biotechnology, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Renal and urogenital, Inflammatory and immune system, Biological Products, Biomarkers, Female, Humans, Interleukin-16, Kidney, Lupus Nephritis, Male, Proteomics, Single-Cell Analysis, Transcriptome, Accelerating Medicines Partnership in Rheumatoid Arthritis and Systemic Lupus Erythematosus Network, Immunology, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectiveCurrent lupus nephritis (LN) treatments are effective in only 30% of patients, emphasizing the need for novel therapeutic strategies. We undertook this study to develop mechanistic hypotheses and explore novel biomarkers by analyzing the longitudinal urinary proteomic profiles in LN patients undergoing treatment.MethodsWe quantified 1,000 urinary proteins in 30 patients with LN at the time of the diagnostic renal biopsy and after 3, 6, and 12 months. The proteins and molecular pathways detected in the urine proteome were then analyzed with respect to baseline clinical features and longitudinal trajectories. The intrarenal expression of candidate biomarkers was evaluated using single-cell transcriptomics of renal biopsy sections from LN patients.ResultsOur analysis revealed multiple biologic pathways, including chemotaxis, neutrophil activation, platelet degranulation, and extracellular matrix organization, which could be noninvasively quantified and monitored in the urine. We identified 237 urinary biomarkers associated with LN, as compared to controls without systemic lupus erythematosus. Interleukin-16 (IL-16), CD163, and transforming growth factor β mirrored intrarenal nephritis activity. Response to treatment was paralleled by a reduction in urinary IL-16, a CD4 ligand with proinflammatory and chemotactic properties. Single-cell RNA sequencing independently demonstrated that IL16 is the second most expressed cytokine by most infiltrating immune cells in LN kidneys. IL-16-producing cells were found at key sites of kidney injury.ConclusionUrine proteomics may profoundly change the diagnosis and management of LN by noninvasively monitoring active intrarenal biologic pathways. These findings implicate IL-16 in LN pathogenesis, designating it as a potentially treatable target and biomarker.

Published
2022

5. Nonlesional lupus skin contributes to inflammatory education of myeloid cells and primes for cutaneous inflammation

Author

Billi, Allison C, Ma, Feiyang, Plazyo, Olesya, Gharaee-Kermani, Mehrnaz, Wasikowski, Rachael, Hile, Grace A, Xing, Xianying, Yee, Christine M, Rizvi, Syed M, Maz, Mitra P, Berthier, Celine C, Wen, Fei, Tsoi, Lam C, Pellegrini, Matteo, Modlin, Robert L, Gudjonsson, Johann E, and Kahlenberg, J Michelle

Subjects
Biomedical and Clinical Sciences, Immunology, Lupus, Genetics, Clinical Research, Autoimmune Disease, 2.1 Biological and endogenous factors, Inflammatory and immune system, Humans, Inflammation, Interferon Type I, Keratinocytes, Lupus Erythematosus, Cutaneous, Myeloid Cells, Biological Sciences, Medical and Health Sciences, Medical biotechnology, Biomedical engineering
Abstract

Cutaneous lupus erythematosus (CLE) is a disfiguring and poorly understood condition frequently associated with systemic lupus. Previous studies suggest that nonlesional keratinocytes play a role in disease predisposition, but this has not been investigated in a comprehensive manner or in the context of other cell populations. To investigate CLE immunopathogenesis, normal-appearing skin, lesional skin, and circulating immune cells from lupus patients were analyzed via integrated single-cell RNA sequencing and spatial RNA sequencing. We demonstrate that normal-appearing skin of patients with lupus represents a type I interferon-rich, prelesional environment that skews gene transcription in all major skin cell types and markedly distorts predicted cell-cell communication networks. We also show that lupus-enriched CD16+ dendritic cells undergo robust interferon education in the skin, thereby gaining proinflammatory phenotypes. Together, our data provide a comprehensive characterization of lesional and nonlesional skin in lupus and suggest a role for skin education of CD16+ dendritic cells in CLE pathogenesis.

Published
2022

7. An integrated organoid omics map extends modeling potential of kidney disease

Author

Lassé, Moritz, El Saghir, Jamal, Berthier, Celine C., Eddy, Sean, Fischer, Matthew, Laufer, Sandra D., Kylies, Dominik, Hutzfeldt, Arvid, Bonin, Léna Lydie, Dumoulin, Bernhard, Menon, Rajasree, Vega-Warner, Virginia, Eichinger, Felix, Alakwaa, Fadhl, Fermin, Damian, Billing, Anja M., Minakawa, Akihiro, McCown, Phillip J., Rose, Michael P., Godfrey, Bradley, Meister, Elisabeth, Wiech, Thorsten, Noriega, Mercedes, Chrysopoulou, Maria, Brandts, Paul, Ju, Wenjun, Reinhard, Linda, Hoxha, Elion, Grahammer, Florian, Lindenmeyer, Maja T., Huber, Tobias B., Schlüter, Hartmut, Thiel, Steffen, Mariani, Laura H., Puelles, Victor G., Braun, Fabian, Kretzler, Matthias, Demir, Fatih, Harder, Jennifer L., and Rinschen, Markus M.

Published
2023
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8. Safety of procuring research tissue during a clinically indicated kidney biopsy from patients with lupus: data from the Accelerating Medicines Partnership RA/SLE Network.

Author

Deonaraine, Kristina K, Carlucci, Philip M, Fava, Andrea, Li, Jessica, Wofsy, David, James, Judith A, Putterman, Chaim, Diamond, Betty, Davidson, Anne, Fine, Derek M, Monroy-Trujillo, Jose, Atta, Mohamed G, Haag, Kristin, Rao, Deepak A, Apruzzese, William, Belmont, H Michael, Izmirly, Peter M, Wu, Ming, Connery, Sean, Payan-Schober, Fernanda, Furie, Richard A, Berthier, Celine C, Dall'Era, Maria, Cho, Kerry, Kamen, Diane L, Kalunian, Kenneth, Anolik, Jennifer, Ishimori, Mariko, Weisman, Michael H, Accelerating Medicines Partnership RA/SLE network, Petri, Michelle A, and Buyon, Jill P

Subjects
Accelerating Medicines Partnership RA/SLE network, autoimmunity, lupus erythematosus, lupus nephritis, systemic
Abstract

ObjectivesIn lupus nephritis the pathological diagnosis from tissue retrieved during kidney biopsy drives treatment and management. Despite recent approval of new drugs, complete remission rates remain well under aspirational levels, necessitating identification of new therapeutic targets by greater dissection of the pathways to tissue inflammation and injury. This study assessed the safety of kidney biopsies in patients with SLE enrolled in the Accelerating Medicines Partnership, a consortium formed to molecularly deconstruct nephritis.Methods475 patients with SLE across 15 clinical sites in the USA consented to obtain tissue for research purposes during a clinically indicated kidney biopsy. Adverse events (AEs) were documented for 30 days following the procedure and were determined to be related or unrelated by all site investigators. Serious AEs were defined according to the National Institutes of Health reporting guidelines.Results34 patients (7.2%) experienced a procedure-related AE: 30 with haematoma, 2 with jets, 1 with pain and 1 with an arteriovenous fistula. Eighteen (3.8%) experienced a serious AE requiring hospitalisation; four patients (0.8%) required a blood transfusion related to the kidney biopsy. At one site where the number of cores retrieved during the biopsy was recorded, the mean was 3.4 for those who experienced a related AE (n=9) and 3.07 for those who did not experience any AE (n=140). All related AEs resolved.ConclusionsProcurement of research tissue should be considered feasible, accompanied by a complication risk likely no greater than that incurred for standard clinical purposes. In the quest for targeted treatments personalised based on molecular findings, enhanced diagnostics beyond histology will likely be required.

Published
2021

10. Contribution of plasma cells and B-cells to hidradenitis suppurativa pathogenesis

Author

Gudjonsson, Johann E, Tsoi, Lam C, Ma, Feiyang, Billi, Allison C, van Straalen, Kelsey R, Vossen, Allard RJV, Zee, HH, Harms, Paul W, Wasikowski, Rachael, Yee, Christine M, Rizvi, Syed Monem, Xing, Xianying, Xing, Enze, Plazyo, Olesya, Zeng, Chang, Patrick, Matthew T, Lowe, Margaret M, Burney, Richard E, Kozlow, Jeffrey H, Cherry-Bukowiec, Jill R, Jiang, Yanyun, Kirma, Joseph, Weidinger, Stephan, Cushing, Kelly C, Rosenblum, Michael D, Berthier, Celine C, MacLeod, Amanda S, Voorhees, John J, Wen, Fei, Kahlenberg, J Michelle, Maverakis, Emanual, Modlin, Robert L, and Prens, Errol P

Subjects
Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Agammaglobulinaemia Tyrosine Kinase, B-Lymphocytes, Biomarkers, Case-Control Studies, Gene Expression Regulation, Gene Regulatory Networks, Hidradenitis Suppurativa, Humans, Plasma Cells, Proteome, Signal Transduction, Single-Cell Analysis, Syk Kinase, Transcriptome, B cells, Complement, Dermatology, Immunology, Skin
Abstract

Hidradenitis suppurativa (HS) is a debilitating chronic inflammatory skin disease characterized by chronic abscess formation and development of multiple draining sinus tracts in the groin, axillae, and perineum. Using proteomic and transcriptomic approaches, we characterized the inflammatory responses in HS in depth, revealing immune responses centered on IFN-γ, IL-36, and TNF, with lesser contribution from IL-17A. We further identified B cells and plasma cells, with associated increases in immunoglobulin production and complement activation, as pivotal players in HS pathogenesis, with Bruton's tyrosine kinase (BTK) and spleen tyrosine kinase (SYK) pathway activation as a central signal transduction network in HS. These data provide preclinical evidence to accelerate the path toward clinical trials targeting BTK and SYK signaling in moderate-to-severe HS.

Published
2020

11. Accelerating Medicines Partnership: Organizational Structure and Preliminary Data From the Phase 1 Studies of Lupus Nephritis

Author

Hoover, Paul, Der, Evan, Berthier, Celine C, Arazi, Arnon, Lederer, James A, James, Judith A, Buyon, Jill, Petri, Michelle, Belmont, H Michael, Izmirly, Peter, Wofsy, David, Hacohen, Nir, Diamond, Betty, Putterman, Chaim, and Davidson, Anne

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Autoimmune Disease, Lupus, Kidney Disease, Clinical Research, Good Health and Well Being, Academic Medical Centers, Biomarkers, Clinical Trials, Phase I as Topic, Drug Industry, Humans, Lupus Nephritis, National Institutes of Health (U.S.), Preliminary Data, Public-Private Sector Partnerships, Sequence Analysis, RNA, United States, Public Health and Health Services, Psychology, Clinical sciences, Allied health and rehabilitation science
Abstract

The Accelerating Medicines Partnership (AMP) Lupus Network was established as a partnership between the National Institutes of Health, pharmaceutical companies, nonprofit stakeholders, and lupus investigators across multiple academic centers to apply high-throughput technologies to the analysis of renal tissue, urine, and blood from patients with lupus nephritis (LN). The AMP network provides publicly accessible data to the community with the goal of generating new scientific hypotheses and improving diagnostic and therapeutic tools so as to improve disease outcomes. We present here a description of the structure of the AMP Lupus Network and a summary of the preliminary results from the phase 1 studies. The successful completion of phase 1 sets the stage for analysis of a large cohort of LN samples in phase 2 and provides a model for establishing similar discovery cohorts.

Published
2020

12. The immune cell landscape in kidneys of patients with lupus nephritis

Author

Arazi, Arnon, Rao, Deepak A, Berthier, Celine C, Davidson, Anne, Liu, Yanyan, Hoover, Paul J, Chicoine, Adam, Eisenhaure, Thomas M, Jonsson, A Helena, Li, Shuqiang, Lieb, David J, Zhang, Fan, Slowikowski, Kamil, Browne, Edward P, Noma, Akiko, Sutherby, Danielle, Steelman, Scott, Smilek, Dawn E, Tosta, Patti, Apruzzese, William, Massarotti, Elena, Dall’Era, Maria, Park, Meyeon, Kamen, Diane L, Furie, Richard A, Payan-Schober, Fernanda, Pendergraft, William F, McInnis, Elizabeth A, Buyon, Jill P, Petri, Michelle A, Putterman, Chaim, Kalunian, Kenneth C, Woodle, E Steve, Lederer, James A, Hildeman, David A, Nusbaum, Chad, Raychaudhuri, Soumya, Kretzler, Matthias, Anolik, Jennifer H, Brenner, Michael B, Wofsy, David, Hacohen, Nir, and Diamond, Betty

Subjects
Biomedical and Clinical Sciences, Immunology, Kidney Disease, Genetics, Autoimmune Disease, Clinical Research, Lupus, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, 4.1 Discovery and preclinical testing of markers and technologies, Inflammatory and immune system, Renal and urogenital, Biomarkers, Biopsy, Cluster Analysis, Computational Biology, Epithelial Cells, Flow Cytometry, Gene Expression Profiling, Gene Expression Regulation, Humans, Immunophenotyping, Interferons, Kidney, Leukocytes, Lupus Nephritis, Lymphocytes, Molecular Sequence Annotation, Myeloid Cells, Single-Cell Analysis, Transcriptome, Accelerating Medicines Partnership in SLE network, Biochemistry and cell biology
Abstract

Lupus nephritis is a potentially fatal autoimmune disease for which the current treatment is ineffective and often toxic. To develop mechanistic hypotheses of disease, we analyzed kidney samples from patients with lupus nephritis and from healthy control subjects using single-cell RNA sequencing. Our analysis revealed 21 subsets of leukocytes active in disease, including multiple populations of myeloid cells, T cells, natural killer cells and B cells that demonstrated both pro-inflammatory responses and inflammation-resolving responses. We found evidence of local activation of B cells correlated with an age-associated B-cell signature and evidence of progressive stages of monocyte differentiation within the kidney. A clear interferon response was observed in most cells. Two chemokine receptors, CXCR4 and CX3CR1, were broadly expressed, implying a potentially central role in cell trafficking. Gene expression of immune cells in urine and kidney was highly correlated, which would suggest that urine might serve as a surrogate for kidney biopsies.

Published
2019

15. Urine Single-Cell RNA Sequencing in Focal Segmental Glomerulosclerosis Reveals Inflammatory Signatures

Author

Latt, Khun Zaw, Heymann, Jurgen, Jessee, Joseph H., Rosenberg, Avi Z., Berthier, Celine C., Arazi, Arnon, Eddy, Sean, Yoshida, Teruhiko, Zhao, Yongmei, Chen, Vicky, Nelson, George W., Cam, Margaret, Kumar, Parimal, Mehta, Monika, Kelly, Michael C., Kretzler, Matthias, Ray, Patricio E., Moxey-Mims, Marva, Gorman, Gregory H., Lechner, Brent L., Regunathan-Shenk, Renu, Raj, Dominic S., Susztak, Katalin, Winkler, Cheryl A., and Kopp, Jeffrey B.

Published
2022
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16. Genome-Wide Association Study in Acute Tubulointerstitial Nephritis

Author

Zhou, Xu-Jie, Su, Tao, Xie, Jingyuan, Xie, Qiong-Hong, Wang, Li-Zhong, Hu, Yong, Chen, Gang, Jia, Yan, Huang, Jun-Wen, Li, Gui, Liu, Yang, Yu, Xiao-Juan, Nath, Swapan K., Tsoi, Lam C., Patrick, Matthew T., Berthier, Celine C., Liu, Gang, Wang, Su-Xia, Xu, Huji, Chen, Nan, Hao, Chuan-Ming, Zhang, Hong, and Yang, Li

Published
2023
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17. SARS-CoV-2 receptor networks in diabetic and COVID-19–associated kidney disease

Author

Menon, Rajasree, Otto, Edgar A., Sealfon, Rachel, Nair, Viji, Wong, Aaron K., Theesfeld, Chandra L., Chen, Xi, Wang, Yuan, Boppana, Avinash S., Luo, Jinghui, Yang, Yingbao, Kasson, Peter M., Schaub, Jennifer A., Berthier, Celine C., Eddy, Sean, Lienczewski, Chrysta C., Godfrey, Bradley, Dagenais, Susan L., Sohaney, Ryann, Hartman, John, Fermin, Damian, Subramanian, Lalita, Looker, Helen C., Harder, Jennifer L., Mariani, Laura H., Hodgin, Jeffrey B., Sexton, Jonathan Z., Wobus, Christiane E., Naik, Abhijit S., Nelson, Robert G., Troyanskaya, Olga G., and Kretzler, Matthias

Published
2020
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20. Epidermal ZBP1 stabilizes mitochondrial Z-DNA to drive UV-induced IFN signaling in autoimmune photosensitivity

Author

Klein, Benjamin, primary, Reynolds, Mack B., additional, Xu, Bin, additional, Gharaee-Kermani, Mehrnaz, additional, Gao, Yiqing, additional, Berthier, Celine C., additional, Henning, Svenja, additional, Loftus, Shannon N., additional, McNeely, Kelsey E., additional, Victory, Amanda M., additional, Dobry, Craig J., additional, Hile, Grace A., additional, Ma, Feiyang, additional, Turnier, Jessica L., additional, Gudjonsson, Johann E., additional, O'Riordan, Mary X., additional, and Kahlenberg, J. Michelle, additional

Published
2024
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21. Urine proteomic signatures of histological class, activity, chronicity, and treatment response in lupus nephritis

Author

Fava, Andrea, primary, Buyon, Jill, additional, Magder, Laurence, additional, Hodgin, Jeff, additional, Rosenberg, Avi, additional, Demeke, Dawit S., additional, Rao, Deepak A., additional, Arazi, Arnon, additional, Celia, Alessandra Ida, additional, Putterman, Chaim, additional, Anolik, Jennifer H., additional, Barnas, Jennifer, additional, Dall’Era, Maria, additional, Wofsy, David, additional, Furie, Richard, additional, Kamen, Diane, additional, Kalunian, Kenneth, additional, James, Judith A., additional, Guthridge, Joel, additional, Atta, Mohamed G., additional, Monroy Trujillo, Jose, additional, Fine, Derek, additional, Clancy, Robert, additional, Belmont, H. Michael, additional, Izmirly, Peter, additional, Apruzzese, William, additional, Goldman, Daniel, additional, Berthier, Celine C., additional, Hoover, Paul, additional, Hacohen, Nir, additional, Raychaudhuri, Soumya, additional, Davidson, Anne, additional, Diamond, Betty, additional, and Petri, Michelle, additional

Published
2024
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25. The Hippo pathway regulates photosensitivity in lupus skin

Author

Hile, Grace A., primary, Coit, Patrick, additional, Xu, Bin, additional, Victory, Amanda M., additional, Gharaee‐Kermani, Mehrnaz, additional, Estadt, Shannon N., additional, Maz, Mitra P., additional, Martens, Jacob W. S., additional, Wasikowski, Rachael, additional, Dobry, Craig, additional, Tsoi, Lam C., additional, Iglesias‐Bartolome, Ramiro, additional, Berthier, Celine C., additional, Billi, Allison C., additional, Gudjonsson, Johann E., additional, Sawalha, Amr H., additional, and Kahlenberg, J. Michelle, additional

Published
2023
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31. Regulation of Photosensitivity by the Hippo Pathway in Lupus Skin.

Author

Hile, Grace A., Coit, Patrick, Xu, Bin, Victory, Amanda M., Gharaee‐Kermani, Mehrnaz, Estadt, Shannon N., Maz, Mitra P., Martens, Jacob W. S., Wasikowski, Rachael, Dobry, Craig, Tsoi, Lam C., Iglesias‐Bartolome, Ramiro, Berthier, Celine C., Billi, Allison C., Gudjonsson, Johann E., Sawalha, Amr H., and Kahlenberg, J. Michelle

Subjects
PHOTOSENSITIVITY disorders, STAINS & staining (Microscopy), HIPPO signaling pathway, LUPUS erythematosus, APOPTOSIS, RNA, DNA methylation, COMPARATIVE studies, GENE expression, IMMUNOBLOTTING, FLUORESCENT antibody technique, TRANSCRIPTION factors, KERATINOCYTES, EPIGENOMICS, CYTOPLASM, DISEASE complications
Abstract

Objective: Photosensitivity is one of the most common manifestations of systemic lupus erythematosus (SLE), yet its pathogenesis is not well understood. The normal‐appearing epidermis of patients with SLE exhibits increased ultraviolet B (UVB)–driven cell death that persists in cell culture. Here, we investigated the role of epigenetic modification and Hippo signaling in enhanced UVB‐induced apoptosis seen in SLE keratinocytes. Methods: We analyzed DNA methylation in cultured keratinocytes from SLE patients compared to keratinocytes from healthy controls (n = 6/group). Protein expression was validated in cultured keratinocytes using immunoblotting and immunofluorescence. An immortalized keratinocyte line overexpressing WWC1 was generated via lentiviral vector. WWC1‐driven changes were inhibited using a large tumor suppressor kinase 1/2 (LATS1/2) inhibitor (TRULI) and small interfering RNA (siRNA). The interaction between the Yes‐associated protein (YAP) and the transcriptional enhancer associate domain (TEAD) was inhibited by overexpression of an N/TERT cell line expressing a tetracycline‐inducible green fluorescent protein–tagged protein that inhibits YAP–TEAD binding (TEADi). Apoptosis was assessed using cleaved caspase 3/7 and TUNEL staining. Results: Hippo signaling was the top differentially methylated pathway in SLE versus control keratinocytes. SLE keratinocytes (n = 6) showed significant hypomethylation (Δβ = −0.153) and thus overexpression of the Hippo regulator WWC1 (P = 0.002). WWC1 overexpression increased LATS1/2 kinase activation, leading to YAP cytoplasmic retention and altered proapoptotic transcription in SLE keratinocytes. Accordingly, UVB‐mediated apoptosis in keratinocytes could be enhanced by WWC1 overexpression or YAP–TEAD inhibition, mimicking SLE keratinocytes. Importantly, inhibition of LATS1/2 with either the chemical inhibitor TRULI or siRNA effectively eliminated enhanced UVB‐apoptosis in SLE keratinocytes. Conclusion: Our work unravels a novel driver of photosensitivity in SLE: overactive Hippo signaling in SLE keratinocytes restricts YAP transcriptional activity, leading to shifts that promote UVB apoptosis. [ABSTRACT FROM AUTHOR]

Published
2023
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32. Publisher Correction: The immune cell landscape in kidneys of patients with lupus nephritis

Author

Arazi, Arnon, Rao, Deepak A., Berthier, Celine C., Davidson, Anne, Liu, Yanyan, Hoover, Paul J., Chicoine, Adam, Eisenhaure, Thomas M., Jonsson, A. Helena, Li, Shuqiang, Lieb, David J., Zhang, Fan, Slowikowski, Kamil, Browne, Edward P., Noma, Akiko, Sutherby, Danielle, Steelman, Scott, Smilek, Dawn E., Tosta, Patti, Apruzzese, William, Massarotti, Elena, Dall’Era, Maria, Park, Meyeon, Kamen, Diane L., Furie, Richard A., Payan-Schober, Fernanda, Pendergraft, III, William F., McInnis, Elizabeth A., Buyon, Jill P., Petri, Michelle A., Putterman, Chaim, Kalunian, Kenneth C., Woodle, E. Steve, Lederer, James A., Hildeman, David A., Nusbaum, Chad, Raychaudhuri, Soumya, Kretzler, Matthias, Anolik, Jennifer H., Brenner, Michael B., Wofsy, David, Hacohen, Nir, Diamond, Betty, and the Accelerating Medicines Partnership in SLE network

Published
2019
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34. B Cell Signatures Distinguish Cutaneous Lupus Erythematosus Subtypes and the Presence of Systemic Disease Activity

Author

Abernathy-Close, Lisa, primary, Lazar, Stephanie, additional, Stannard, Jasmine, additional, Tsoi, Lam C., additional, Eddy, Sean, additional, Rizvi, Syed M., additional, Yee, Christine M., additional, Myers, Emily M., additional, Namas, Rajaie, additional, Lowe, Lori, additional, Reed, Tamra J., additional, Wen, Fei, additional, Gudjonsson, Johann E., additional, Kahlenberg, J. Michelle, additional, and Berthier, Celine C., additional

Published
2021
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39. Comparison of Lesional Juvenile Myositis and Lupus Skin Reveals Overlapping Yet Unique Disease Pathophysiology

Author

Turnier, Jessica L., primary, Pachman, Lauren M., additional, Lowe, Lori, additional, Tsoi, Lam C., additional, Elhaj, Sultan, additional, Menon, Rajasree, additional, Amoruso, Maria C., additional, Morgan, Gabrielle A., additional, Gudjonsson, Johann E., additional, Berthier, Celine C., additional, and Kahlenberg, J. Michelle, additional

Published
2021
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40. SARS-CoV-2 receptor networks in diabetic kidney disease, BK-Virus nephropathy and COVID-19 associated acute kidney injury

Author

Menon, Rajasree, Otto, Edgar A, Sealfon, Rachel, Nair, Viji, Wong, Aaron K, Theesfeld, Chandra L, Chen, Xi, Wang, Yuan, Boppanna, Avinash, Kasson, Peter M, Schaub, Jennifer A, Berthier, Celine C, Eddy, Sean, Lienczewski, Chrysta C, Godfrey, Bradley, Dagenais, Susan L, Sohaney, Ryann, Hartman, John, Fermin, Damian, Subramanian, Lalita, Looker, Helen C, Mariani, Laura H, Naik, Abhijit S, Nelson, Robert G, Troyanskaya, Olga G., and Kretzler, Matthias

Subjects
hormones, hormone substitutes, and hormone antagonists
Abstract

COVID-19 morbidity and mortality is significantly increased in patients with diabetes and kidney disease via unknown mechanisms. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) for entry into human host cells, and ACE2 levels in target cells may influence SARS-CoV-2 susceptibility. We investigated how pre-existing conditions and drug treatments alter receptor expression in kidney tissue. Using single cell RNA profiling (scRNAseq) to assess ACE2 and associated SARS-CoV-2 proteases in healthy living donors (LD) kidneys, diabetic kidney disease (DKD), and in kidney injury during viral infection, ACE2 expression was primarily associated with proximal tubular epithelial cells (PTEC). ACE2 mRNA expression levels were significantly upregulated in DKD versus LD, however, ACE2 levels were not altered by exposures to renin angiotensin aldosterone system (RAAS) inhibitors. ACE2+ expression signatures were defined by differential expression analysis and characterized by Bayesian integrative analysis of a large compendium of public -omics datasets, resulting in the identification of network modules induced in ACE2 positive PTEC in DKD and BK virus nephropathy. These ACE2 upregulated cell programs were linked to viral entry, immune activation, endomembrane reorganization, and RNA processing and overlapped significantly with the cellular responses induced by SARS-CoV-2 infection. Similar cellular programs were activated in ACE2-positive PTEC isolated in a urine sample from a COVID19 patient with acute kidney injury, suggesting a consistent ACE2-coregulated expression program that may interact with SARS-Cov-2 infection processes. The SARS-CoV-2 receptor associated gene signatures could seed further research into therapeutic strategies for COVID-19. Functional networks of gene expression signatures are available for further exploration to researchers at HumanBase (hb.flatironinstitute.org/covid-kidney).

Published
2020
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41. Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: Predictors of pathology and RAS blockade effects

Author

Eid, Stephanie A., primary, Hinder, Lucy M., additional, Zhang, Hongyu, additional, Eksi, Ridvan, additional, Nair, Viji, additional, Eddy, Sean, additional, Eichinger, Felix, additional, Park, Meeyoung, additional, Saha, Jharna, additional, Berthier, Celine C., additional, Jagadish, Hosagrahar V., additional, Guan, Yuanfang, additional, Pennathur, Subramaniam, additional, Hur, Junguk, additional, Kretzler, Matthias, additional, Feldman, Eva L., additional, and Brosius, Frank C., additional

Published
2021
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42. Exome Chip Analyses and Genetic Risk for IgA Nephropathy among Han Chinese

Author

Zhou, Xu-jie, primary, Tsoi, Lam C., additional, Hu, Yong, additional, Patrick, Matthew T., additional, He, Kevin, additional, Berthier, Celine C., additional, Li, Yanming, additional, Wang, Yan-na, additional, Qi, Yuan-yuan, additional, Zhang, Yue-miao, additional, Gan, Ting, additional, Li, Yang, additional, Hou, Ping, additional, Liu, Li-jun, additional, Shi, Su-fang, additional, Lv, Ji-cheng, additional, Xu, Hu-ji, additional, and Zhang, Hong, additional

Published
2021
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43. IL18-containing 5-gene signature distinguishes histologically identical dermatomyositis and lupus erythematosus skin lesions

Author

Tsoi, Lam C., primary, Gharaee-Kermani, Mehrnaz, additional, Berthier, Celine C., additional, Nault, Tori, additional, Hile, Grace A., additional, Estadt, Shannon N., additional, Patrick, Matthew T., additional, Wasikowski, Rachael, additional, Billi, Allison C., additional, Lowe, Lori, additional, Reed, Tamra J., additional, Gudjonsson, Johann E., additional, and Kahlenberg, J. Michelle, additional

Published
2020
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44. Integrated urine proteomics and renal single-cell genomics identify an IFN-γ response gradient in lupus nephritis

Author

Fava, Andrea, primary, Buyon, Jill, additional, Mohan, Chandra, additional, Zhang, Ting, additional, Belmont, H. Michael, additional, Izmirly, Peter, additional, Clancy, Robert, additional, Trujillo, Jose Monroy, additional, Fine, Derek, additional, Zhang, Yuji, additional, Magder, Laurence, additional, Rao, Deepak A., additional, Arazi, Arnon, additional, Berthier, Celine C., additional, Davidson, Anne, additional, Diamond, Betty, additional, Hacohen, Nir, additional, Wofsy, David, additional, Apruzzese, William, additional, Raychaudhuri, Soumya, additional, and Petri, Michelle, additional

Published
2020
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46. SARS-CoV-2 receptor networks in diabetic and COVID-19 associated kidney disease

Author

Menon, Rajasree, primary, Otto, Edgar A., additional, Sealfon, Rachel, additional, Nair, Viji, additional, Wong, Aaron K., additional, Theesfeld, Chandra L., additional, Chen, Xi, additional, Wang, Yuan, additional, Boppana, Avinash S., additional, Luo, Jinghui, additional, Yang, Yingbao, additional, Kasson, Peter M., additional, Schaub, Jennifer A., additional, Berthier, Celine C., additional, Eddy, Sean, additional, Lienczewski, Chrysta C., additional, Godfrey, Bradley, additional, Dagenais, Susan L., additional, Sohaney, Ryann, additional, Hartman, John, additional, Fermin, Damian, additional, Subramanian, Lalita, additional, Looker, Helen C., additional, Harder, Jennifer L., additional, Mariani, Laura H., additional, Hodgin, Jeffrey B., additional, Sexton, Jonathan Z., additional, Wobus, Christiane E., additional, Naik, Abhijit S., additional, Nelson, Robert G., additional, Troyanskaya, Olga G., additional, and Kretzler, Matthias, additional

Published
2020
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47. Single cell transcriptomics identifies focal segmental glomerulosclerosis remission endothelial biomarker

Author

Menon, Rajasree, primary, Otto, Edgar A., additional, Hoover, Paul, additional, Eddy, Sean, additional, Mariani, Laura, additional, Godfrey, Bradley, additional, Berthier, Celine C., additional, Eichinger, Felix, additional, Subramanian, Lalita, additional, Harder, Jennifer, additional, Ju, Wenjun, additional, Nair, Viji, additional, Larkina, Maria, additional, Naik, Abhijit S., additional, Luo, Jinghui, additional, Jain, Sanjay, additional, Sealfon, Rachel, additional, Troyanskaya, Olga, additional, Hacohen, Nir, additional, Hodgin, Jeffrey B., additional, Kretzler, Matthias, additional, and (KPMP), Kidney Precision Medicine Project, additional

Published
2020
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49. The Death Ligand TRAIL in Diabetic Nephropathy

Author

Lorz, Corina, Benito-Marti[Combining Acute Accent]n, Alberto, Boucherot, Anissa, Ucero, Alvaro C., Rastaldi, Maria Pia, Henger, Anna, Armelloni, Silvia, Santamari[Combining Acute Accent]a, Beatriz, Berthier, Celine C., Kretzler, Matthias, Egido, Jesus, and Ortiz, Alberto

Published
2008
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50. IFN-γ enhances cell-mediated cytotoxicity against keratinocytes via JAK2/STAT1 in lichen planus

Author

Shao, Shuai, primary, Tsoi, Lam C., additional, Sarkar, Mrinal K., additional, Xing, Xianying, additional, Xue, Ke, additional, Uppala, Ranjitha, additional, Berthier, Celine C., additional, Zeng, Chang, additional, Patrick, Matthew, additional, Billi, Allison C., additional, Fullmer, Joseph, additional, Beamer, Maria A., additional, Perez-White, Bethany, additional, Getsios, Spiro, additional, Schuler, Andrew, additional, Voorhees, John J., additional, Choi, Sung, additional, Harms, Paul, additional, Kahlenberg, J. Michelle, additional, and Gudjonsson, Johann E., additional

Published
2019
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