Dr. Fairfax studies the immune system response to infection by the parasitic worm Schistosoma mansoni, which is a blood fluke that causes schistosomiasis.
Keke Fairfax, Ph.D.
Assistant Professor of Parasitology (Purdue University)
Dr. Fairfax studied at the University of Chicago for her undergraduate degree and earned her Ph.D. from Yale in 2009. She held postdoctoral positions at the Trudeau Institute (an immunology-focused research center in Upstate New York) and at Washington University in St. Louis. She was briefly an instructor at Wash U after finishing her postdoc, and was hired at Purdue in 2014. She is currently a member of the Department of Comparative Pathobiology at the Purdue’s College of Veterinary Medicine.
White blood cells make up an important component of the immune system, with many subtypes playing specialized roles. When a pathogen enters the body, it will produce foreign proteins, sugars, and fats that can be recognized as antigens (non-self molecules). These antigens will be internalized by antigen-presenting cells, which will display the foreign substance to the B and T cells of the adaptive immune system. One kind of T cell — the T-helper cell — is activated by binding an antigen. It then divides and releases chemicals called cytokines that trigger other responses from the immune system, based on what kind of antigen it recognized.
In a recent paper, Dr. Fairfax and colleagues from her postdoc examined how one type of antigen-presenting cell responds to helminth (worm) infection, by comparing mice that had all of the normal antigen-presenting cells to mice that were missing that specific type. They found that mice that were missing these cells had a stronger immune response to the worms, suggesting that these cells suppress the immune response to infection. On closer inspection, they traced this phenomenon back to a cytokine called IL-12, which is made constantly by the antigen-presenting cells (i.e. not in response to infection/antigen) and which blocks formation of the category of T-helper cells that fights worm infections.
This has important implications for developing new treatments for helminth infections in humans. While previous research had shown that certain antigen-presenting cells help increase the immune response to parasitic worms, it was not known what other cells suppressed this response. It is likely not enough to enhance/encourage the anti-worm response through medication, but also to reduce the opposing (anti-anti-worm) response as well.