Ana Carrizosa Anderson is a Colombian-American microbiologist who is a professor at the Harvard Medical School. Her research combines transcriptomics and systems biology to understand T-cell response to chronic disease.
Ana Carrizosa Anderson | |
|---|---|
| Born | |
| Alma mater | Harvard University University of Miami |
| Scientific career | |
| Institutions | Harvard University |
| Thesis | T cell cross-reactivity in the selection and expansion of the autoreactive T cell repertoire (1999) |
| Website | Ana Anderson Lab |
Early life and education
editAnderson was born in Bogotá.[1] She grew up in Miami, and eventually attended the University of Miami. Anderson studied microbiology and immunology as an undergraduate degree.[2] She moved to Harvard University for her doctoral research, where she studied T cell cross reactivity.[3][4]
Research and career
editAnderson looks to understand the pathways that are involved with T cell response to chronic disease. She has explored the role of regulatory T cells in cancer, and the specific effector T cells in tumor tissue.[5] Her research combines mass cytometry, transcriptomics, and genome editing. Checkpoint receptors regulate the activation, differentiation and function of T-cells. They are up-regulated (e.g. increases response) on activated T cells to mitigate for uncontrolled inflammation. Immune checkpoint receptors are hijacked in cancer, where their high rates of expression on tumor T cells hampers the anti-tumor response. Anderson has investigated TIM-3, an immune checkpoint receptor that is involved with immunity to tumors.[2] The blockade of immune checkpoint receptors is a recognized form of cancer treatment. Anderson is interested in how TIM-3 is involved with regulating tumor tissue immune cells, and understanding how the blockade impacts immune cell function in the tumor microenvironment.[3]
Anderson uses transcriptomics technologies and systems biology to understand dysfunctional T-cells.[citation needed]
Anderson looks to understand the function of Treg in tumor tissue. CD4+FoxP3+ Treg are immunosuppressive cells that suppress anti-tumor immunity. Inside tumor cells, Treg cells up-regulate checkpoint receptors and are major suppressors of anti-tumor immunity. The Treg cells that infiltrate tumor tissue up-regulate immune checkpoint receptors and have a highly suppressive phenotype.[citation needed]
Selected publications
edit- Chen Zhu; Ana C Anderson; Anna Schubart; et al. (December 2005). "The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity". Nature Immunology. 6 (12): 1245–52. doi:10.1038/NI1271. ISSN 1529-2908. PMID 16286920. Wikidata Q28281686.
- Kaori Sakuishi; Lionel Apetoh; Jenna M Sullivan; Bruce R Blazar; Vijay K Kuchroo; Ana C Anderson (6 September 2010). "Targeting Tim-3 and PD-1 pathways to reverse T cell exhaustion and restore anti-tumor immunity". Journal of Experimental Medicine. 207 (10): 2187–2194. doi:10.1084/JEM.20100643. ISSN 0022-1007. PMC 2947065. PMID 20819927. Wikidata Q34161493.
- Ana C Anderson; Nicole Joller; Vijay K Kuchroo (1 May 2016). "Lag-3, Tim-3, and TIGIT: Co-inhibitory Receptors with Specialized Functions in Immune Regulation". Immunity. 44 (5): 989–1004. doi:10.1016/J.IMMUNI.2016.05.001. ISSN 1074-7613. PMC 4942846. PMID 27192565. Wikidata Q38837469.
References
edit- ^ "ACA LAB". ACA LAB. Retrieved 2024-08-12.
- ^ a b "Ana Anderson – CSHL WiSE". Retrieved 2024-08-12.
- ^ a b "Ana Anderson". @broadinstitute. 2019-01-23. Retrieved 2024-08-12.
- ^ "Ana C. Anderson - Committee Member at The Brigham And Women's Hospital, Inc". THE ORG. Retrieved 2024-08-12.
- ^ "Cancer Immunology Program - The Gene Lay Institute". 2024-03-11. Retrieved 2024-08-12.