Nina Papavasiliou is an immunologist and Helmholtz Professor in the Division of Immune Diversity at the
German Cancer Research Center in Heidelberg, Germany. She is also an adjunct professor at the
Rockefeller University, where she was previously associate professor and head of the Laboratory of Lymphocyte Biology. She is best known for her work in the fields of
DNA and
RNA editing.
Education and early career
Papavasiliou received her Bachelors of Science from
Oberlin College in biology in 1992. She then completed her PhD at the
Rockefeller University in
Michel C. Nussenzweig's Laboratory of Molecular Immunology. There, she began studying how
B cell antigen receptors—or
antibodies anchored to the cell membrane—undergo mutation so they can specifically recognize a particular
antigen and elicit an immune response.[1][2] She followed that interest to the
Yale School of Medicine, where she worked as a postdoctoral fellow in the lab of David G. Schatz.[3][4]
Research
Papavasiliou's research centers on demystifying how cells and organisms diversify and expand the information encoded in their genomes, both at the DNA and RNA level. She opened her Laboratory of Lymphocyte Biology at
Rockefeller University in 2001 as an assistant professor.[5] Much of her group's early work was done in the context of the
adaptive immune response, which is able to combat a wide array of pathogens seeking to invade the host by rapidly generating novel antibodies that are able to specifically recognize a given invader. Her group has worked to characterize the activity of an
enzyme known as
activation-induced cytidine deaminase (AID).[6][7] AID changes
cytidine (C) residues to
uracil (U) in DNA, which is recognized as DNA damage and repaired in such a way that introduces
thymidine (T), effectively mutating Cs to Ts in DNA. The process is known as
somatic hypermutation and is how
B cells can rapidly introduce DNA mutations into receptors that recognize the invaders, known as
antigens. Papavasiliou's lab has worked to understand how AID expression is regulated in the immune system and how AID targets certain genes for mutation.[8][9][10]
Papavasiliou also studies
RNA editing in the context of the
innate immune response using
next-generation sequencing and
bioinformatics approaches to identify and characterize RNA editing targets. Her group first identified novel RNA editing targets of
APOBEC1, which mutates a
cytosine to a
uracil in an RNA transcript, and was previously thought to only edit
Apolipoprotein B (apoB) in the small intestine.[11] Her group has since moved on to attempt to characterize the potential role APOBEC1-editing may be playing outside of its function with apoB.[12]
Papavasiliou most recently branched out to studying mechanisms of
antigenic variation—or how pathogens vary their surface proteins to escape the immune response—using
Trypanosoma brucei, the parasite that causes
African sleeping sickness, as a model organism. Her group has developed new tools to better understand the dynamics of protein coat switching in trypanosomes, and is working to better understand the mechanisms by which trypanosomes are able to diversify their coat proteins over the course of an infection.[13][14][15]
^Papavasiliou, Fotini; Jankovic, Mila; Gong, Shiaoching; Nussenzweig, Michel C. (1997-04-01). "Control of immunoglobulin gene rearrangements in developing B cells". Current Opinion in Immunology. 9 (2): 233–238.
doi:
10.1016/S0952-7915(97)80141-0.
ISSN0952-7915.
PMID9099793.
^Papavasiliou, Fotini; Casellas, Rafael; Suh, Heikyung; Qin, Xiao-Feng; Besmer, Eva; Pelanda, Roberta; Nemazee, David; Rajewsky, Klaus; Nussenzweig, Michel C. (1997-10-10). "V(D)J Recombination in Mature B Cells: A Mechanism for Altering Antibody Responses". Science. 278 (5336): 298–301.
doi:
10.1126/science.278.5336.298.
ISSN0036-8075.
PMID9323210.
^Papavasiliou, F. Nina; Schatz, David G. (November 2000). "Cell-cycle-regulated DNA double-strand breaks in somatic hypermutation of immunoglobulin genes". Nature. 408 (6809): 216–221.
doi:
10.1038/35041599.
ISSN0028-0836.
PMID11089977.
S2CID4407389.