
Research Topics
Dr. Kemper’s laboratory investigates how the intracellularly active complement system, the complosome, regulates fundamental cellular processes in health and disease, with the goal of identifying new therapeutic targets for inflammation-driven conditions.
Complement is best known as a circulating arm of innate immunity that detects and eliminates pathogens. Research from Dr. Kemper’s laboratory discovered that complement is not confined to the bloodstream or cell surface. Instead, key components, including C3 and C5, are activated inside immune cells, forming an intracellular system termed the “complosome.” This discovery revealed that complement directly regulates the behavior of individual cells from within, influencing metabolism, mitochondrial function, gene transcription, and inflammatory responses. In T cells, intracellular complement activity determines differentiation and the intensity and resolution of inflammation; in monocytes and macrophages, it controls production of highly inflammatory cytokines. Further, perturbations in cell-intrinsic and/or intracellular complement functions are associated with a range of human inflammatory pathogenicities.
These findings fundamentally changed the view of complement, from a circulating defense system that targets pathogens to a dynamic, cell-intrinsic regulator of cellular function and tissue integrity – and argues that cell-intrinsic complement may provide new therapeutic targets for inflammation-driven and immune-mediated diseases.
Dr. Kemper’s research program aims at understanding the biology of intracellular complement and how it can be targeted to reduce human disease.
The laboratory is actively engaged in NIH cross-institutional initiatives and combines human genetics with studies of immune and tissue cells from healthy donors and patients with complement deficiencies, infection, autoimmune disease, cancer, and complosome-associated disorders. Multiomic approaches, including transcriptomic, single-cell RNA, epigenetic, spatial proteomic, and metabolomic analyses, are integrated with mechanistic in vitro studies and mouse models to establish biological significance and advance preclinical drug development. Current disease foci include:
1. Lung pathologies including asthma, chronic infection and fibrosis
2. Vascular inflammation impacting CNS functions
3. Cancer (prostate cancer and neuroblastoma)
Biography
Dr. Kemper is a senior investigator and section chief at the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health (NIH), in Bethesda, Maryland.
She received her Ph.D. in 1998 from the Bernhard Nocht Institute for Tropical Medicine in Germany and joined John Atkinson’s laboratory at Washington University in St. Louis as a postdoctoral fellow in 1999. There, she identified the complement regulator and receptor CD46 as an unexpected key checkpoint in the induction of human Th1 responses.
In 2008, Dr. Kemper moved to King’s College London, where her group discovered the intracellularly active complement system, or “complosome.” The complosome performs noncanonical functions in cell biology, including the regulation of key metabolic pathways, mitochondrial dynamics and quality control, and gene transcription. Her group subsequently demonstrated that perturbations of cell-intrinsic and intracellularly active complement components are associated with a range of human diseases, including primary immunodeficiency, arthritis, cardiovascular disease, and cancer.
Dr. Kemper is the recipient of a Wellcome Trust Investigator Award, the Merit Award for Excellence in Science from the International Complement Society, and two Orloff Awards in Science from NHLBI/NIH. She is an elected member of the Henry Kunkel Society and the Medical Research Club London (MRC). She serves on the Scientific Board of Apellis, Inc., and previously served as the elected president of the International Complement Society (ICS). She currently serves as the elected co-chair of the Nomenclature Committee and the Publication Committee of the International Union of Immunological Societies (IUIS).
Selected Publications
- Singh P, Wang L, Ramdas P, Jayasundara SM, Le Friec G, Kunz N, Mudvari P, West EE, Case A, Merle NS, Bibby JA, Hasle H, Boritz EA, Kazemian M, Kemper C. Sp1 links CD46 to CD4 T cell metabolic fitness, survival, and retroviral control. Sci Immunol. 2026;11(121):eaeb5857.
- Rahman J, Bibby JA, Singh P, Merle NS, West EE, Bohrer A, Mayer-Barber K, Liu C, Brinster LR, Afzali B, Briones AM, Alehashemi S, Bhuyan F, Ge J, Chen X, Zhou Y, Clarke MCH, Liu B, Goldbach-Mansky R, Serezani CH, Kemper C. A CD4(+) T cell-intrinsic complement C5aR2-prostacyclin-IL-1R2 axis orchestrates Th1 cell contraction. Immunity. 2025;58(6):1438-1455.e10.
- West EE, Merle NS, Kamiński MM, Palacios G, Kumar D, Wang L, Bibby JA, Overdahl K, Jarmusch AK, Freeley S, Lee DY, Thompson JW, Yu ZX, Taylor N, Sitbon M, Green DR, Bohrer A, Mayer-Barber KD, Afzali B, Kazemian M, Scholl-Buergi S, Karall D, Huemer M, Kemper C. Loss of CD4(+) T cell-intrinsic arginase 1 accelerates Th1 response kinetics and reduces lung pathology during influenza infection. Immunity. 2023;56(9):2036-2053.e12.
- West EE, Woodruff T, Fremeaux-Bacchi V, Kemper C. Complement in human disease: approved and up-and-coming therapeutics. Lancet. 2024;403(10424):392-405.
- Arbore G, West EE, Spolski R, Robertson AAB, Klos A, Rheinheimer C, Dutow P, Woodruff TM, Yu ZX, O'Neill LA, Coll RC, Sher A, Leonard WJ, Köhl J, Monk P, Cooper MA, Arno M, Afzali B, Lachmann HJ, Cope AP, Mayer-Barber KD, Kemper C. T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4⁺ T cells. Science. 2016;352(6292):aad1210.
Related Scientific Focus Areas
This page was last updated on Thursday, October 8, 2026


