PI3Kα in the pathogenesis and treatment of lupus nephritis.
Kasinath, Vivek, and George C Tsokos. 2024. “PI3Kα in the Pathogenesis and Treatment of Lupus Nephritis.”. Kidney International.
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Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.
Umeda, Masataka, Kohei Karino, Abhigyan Satyam, Nobuya Yoshida, Ryo Hisada, Rhea Bhargava, Theodoros Vichos, et al. 2024. “Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.”. Arthritis & Rheumatology (Hoboken, N.J.).
The Role of Podocytes in Lupus Pathology.
Maeda, Kayaho, Reza Abdi, and George C Tsokos. 2024. “The Role of Podocytes in Lupus Pathology.”. Current Rheumatology Reports 27 (1): 10.
The ubiquitin E3 ligase TRIM21 suppresses type I interferon signaling via STING degradation and ameliorates systemic autoimmunity.
Kim, Da Som, Youngjae Park, George C Tsokos, Mi- La Cho, and Seung-Ki Kwok. 2025. “The Ubiquitin E3 Ligase TRIM21 Suppresses Type I Interferon Signaling via STING Degradation and Ameliorates Systemic Autoimmunity.”. Experimental & Molecular Medicine.
Aberrant Glycosylation of IgG in Children With Active Lupus Nephritis Alters Podocyte Metabolism and Causes Podocyte Injury.
Bhargava, Rhea, Rohit Upadhyay, Cong Zhao, Prasad Katakam, Scott Wenderfer, Jing Chen, Hua He, Richard Cummings, Maria G Tsokos, and George C Tsokos. 2025. “Aberrant Glycosylation of IgG in Children With Active Lupus Nephritis Alters Podocyte Metabolism and Causes Podocyte Injury.”. Arthritis & Rheumatology (Hoboken, N.J.).
Calcium calmodulin kinase IV deficiency in podocytes prevents the development of lupus nephritis.
Bhargava, Rhea, Hao Li, Kayaho Maeda, Maria G Tsokos, and George C Tsokos. 2025. “Calcium Calmodulin Kinase IV Deficiency in Podocytes Prevents the Development of Lupus Nephritis.”. Clinical Immunology (Orlando, Fla.) 271: 110427.
Dysregulated soluble immune mediators and lupus-associated autoantibody specificities inform the development of immune indexes that characterise classified SLE transition and SLE disease activity.
Munroe, Melissa E, Kendra Young, Rufei Lu, Joel M Guthridge, Diane L Kamen, Gary S Gilkeson, Michael H Weisman, et al. 2025. “Dysregulated Soluble Immune Mediators and Lupus-Associated Autoantibody Specificities Inform the Development of Immune Indexes That Characterise Classified SLE Transition and SLE Disease Activity.”. Lupus Science & Medicine 12 (2).
IL-17+/IL-10+ Ratio in TCRαβ+ CD4- CD8- T Cells As a Marker of Disease Activity in Lupus-Prone Mice and Patients With Systemic Lupus Erythematosus.
Imai, Rui, Yi Li, Hao Li, Anwesha Kar, Rong Fu, Wei Li, Vasileios C Kyttaris, and George C Tsokos. 2025. “IL-17+/IL-10+ Ratio in TCRαβ+ CD4- CD8- T Cells As a Marker of Disease Activity in Lupus-Prone Mice and Patients With Systemic Lupus Erythematosus.”. ACR Open Rheumatology 7 (10): e70108.
Interleukin-23 receptor deficiency in podocytes averts the development of lupus nephritis.
Fu, Rong, Afroditi Boulougoura, Shuilian Yu, Hao Li, Wenliang Pan, Yushiro Endo, Rhea Bhargava, et al. 2025. “Interleukin-23 Receptor Deficiency in Podocytes Averts the Development of Lupus Nephritis.”. Arthritis & Rheumatology (Hoboken, N.J.).
ADAM9 Promotes Glycolysis in Th17 Cells and Autoimmunity Through Activation of IGF-1 Signaling.
Karino, Kohei, Masataka Umeda, Theodoros Vichos, Wenliang Pan, Michihito Kono, Maria G Tsokos, and George C Tsokos. 2025. “ADAM9 Promotes Glycolysis in Th17 Cells and Autoimmunity Through Activation of IGF-1 Signaling.”. Arthritis & Rheumatology (Hoboken, N.J.).