Faculty Profile

Bio-Robin Stephens

  • Malaria still kills almost 1 million people a year, mostly children in sub-Saharan Africa. Vaccine work has entered a very hopeful stage, but very little is known about the factors determining immunity to this disease caused by protozoan parasites of the genus Plasmodium. Dr. Stephens’ laboratory focuses on the immunology and pathology of malaria infection using the P. chabaudi parasite. Both B and T cells are required for full clearance of the parasite, which can become chronic if this adaptive response is not successful. Her recent work has defined protective CD4 T cell subsets in both the effector and memory T cell compartments. She has also defined a differentiation pathway for generation of these protective subsets, including a metabolic pathway required for successful generation of CD4 memory T cells. She recently discovered a unique hybrid T cell type that has biomarkers of both Th1 and Tfh cells in malaria. Therefore, her ongoing work concerns the mechanisms of differentiation of these protective subsets, and how the hybrid Th1/Tfh T cells provide help for B cells to make antibodies to clear the infection. She is also studying the role of inflammatory tissue pathology in malaria disease. In future work, she plans to design vaccine strategies to generate the protective CD4 T cell subsets for optimal effectiveness.

  • Medical / Professional:

    Cornell University, Ithaca, NY, B.A., 1993

    New York University, New York, NY, M.S., 1997

    Washington University, St. Louis, MO, Ph.D., 2001

    Post Doctoral:

    National Institute for Medical Research, London, England, 2010

  1. The contribution of Plasmodium chabaudi to our understanding of malaria.
    Stephens R, Culleton RL, Lamb TJ.
    Trends in parasitology. 2012; 28(2):73-82. PMID:
  2. Early Decision: Effector and Effector Memory T Cell Differentiation in Chronic Infection.
    Opata MM, Stephens R.
    Current immunology reviews. 2013; 9(3):190-206. PMID:
  3. IFN-γ and IL-21 Double Producing T Cells Are Bcl6-Independent and Survive into the Memory Phase in Plasmodium chabaudi Infection.
    Carpio VH, Opata MM, Montañez ME, Banerjee PP, Dent AL, Stephens R.
    PloS one. 2015; 10(12):e0144654. PMID:
  4. Early effector cells survive the contraction phase in malaria infection and generate both central and effector memory T cells.
    Opata MM, Carpio VH, Ibitokou SA, Dillon BE, Obiero JM, Stephens R.
    Journal of immunology . 2015; 194(11):5346-54. PMID:
  5. Effector memory Th1 CD4 T cells are maintained in a mouse model of chronic malaria.
    Stephens R, Langhorne J.
    PLoS pathogens. 2010; 6(11):e1001208. PMID:
Degree/Training CompletedYearName & Location
B.A.1993Cornell University, Ithaca, NY
M.S.1997New York University, New York, NY
Ph.D.2001Washington University, St. Louis, MO
Post Doctoral2010National Institute for Medical Research, London, England