Senior Investigator
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Senior Investigator, Program in Cellular and Molecular Medicine Professor of Pediatrics, Harvard Medical School |
Dr. Michael Carroll received his Ph.D. in Immunology from the UT Southwestern Medical School (Dallas, TX) under the direction of Dr. J. Donald Capra; subsequently, he trained with Dr. Rodney R. Porter in the Biochemistry Department, Oxford U (Oxford UK). In 1985, he was appointed an Assistant Professor in Pediatrics and the Department of Biological Chemistry at the Children’s Hospital/Harvard Medical School. He was promoted in 1998 to the rank of Professor of Pediatrics, Harvard Medical School and Senior Investigator, Boston Children’s Hospital, Program in Cellular and Molecular Medicine.
Dr. Carroll served as Director of the Harvard Graduate Program in Immunology from 2005 – 2016. Early in his career, he was an American Arthritis Foundation Fellow and Investigator and later a recipient of a Pew Scholar award. He is a recipient of the 2016 Research Award by National Alliance for Mental Health.
A major focus of his research is understanding how autoreactive germinal centers are regulated; and how peripheral autoimmunity can affect neuropsychiatric behavior. Moreover, his research includes understanding how changes in the regulation of the complement system in the brain can underlie diseases such as schizophrenia.
Staff
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Elisabeth Carroll, PharmD DPharm University Paul Sabatier Toulouse, France Administrative Assistant /Lab Manager/Senior Research Associate Email: Elisabeth.carroll@childrens.harvard.edu Alpert Building, 617.713.8714 |
Postdoctoral Fellows
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Kristine Oleinika, PhD Activated B cells can participate in the extrafollicular or the germinal centre response, which differ in their functional output. I am interested in understanding the molecular cues and cellular interactions that guide B cell fate decisions following activation. It remains unclear to what extent overlap exists between pathways that contribute to autoimmunity and protective immunity (such as in response to infection or vaccination). Enhanced understanding of this may allow to design improved intervention strategies for autoimmunity. |
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Anuj Rattan, PhD Generation of autoantibodies by auto reactive B cells is one of the major hallmarks of autoimmunity. Apoptotic cells are major source of autoantigens and inefficient clearance of apoptotic cells is central to activation of auto reactive B cells. I am interested in understanding the role of a newly identified complement receptor, NRP1 (CD304) in apoptotic cell clearance (immune complexes) and its implication in regulation of autoimmunity. |
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Yingying Zhang, PhD By applying a newly developed technology called MERFISH (Multiplexed Error Robust Fluorescent in-situ Hybridization), I am interested in addressing the following questions: 1) which brain cell types express complement components? 2) where in the brain and when during development are they expressed? 3) how does C4 deficiency or C4 overexpression affect the transcriptional landscape in the mouse brain? The ultimate goal is to understand the role of C4 and the complement pathway during brain development and how mechanistically C4 overexpression can contribute to schizophrenia. |
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Chunzhu Song I will focus on identifying cellular and molecular mechanisms of TFN-I-related synaptic elimination and behavior changes in the CNS of a lupus model. |
Graduate Students
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Elliot Akama-Garren I am interested in self-reactive T cells and how they are regulated especially in epitope spreading in systemic autoimmunity. |
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Stacie Lin I am interested in immune mediators localized to the meninges and blood brain barrier driving neurological manifestations in autoimmunity and infection. |
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Danni Zhu I am interested in understanding the mechanisms behind persistent autoantibody production in SLE and how innate immune sensors regulate autoreactive memory B cell activity. |
Research Staff
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Diana Pascual Animal Technician |
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Yilin Guan My project is to elucidate the role of Complement C4 in brain ventricle enlargement and choroid plexus homeostasis. |
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Finley Lord Rescuing schizophrenia-like phenotypes by inhibiting complement overactivation in a mouse model. |
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Ha Lee Undergraduate Student, Harvard University Email: Ha.lee@ childrens.harvard.edu
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Selma Mouftakir MD Student, Karolinska Institute, Stockholm Email: Selma.mouftakir@ childrens.harvard.edu
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