Richard T Robinson, PhD
Microbiology and Molecular Genetics
Medical College of Wisconsin
Research Focus: Cellular Responses to Mycobacterium tuberculosis
PhD: Dartmouth College (2007)
Postdoctoral Training: Trudeau Institute, Saranac Lake, NY
An estimated one third of the world’s population has been exposed to Mycobacterium tuberculosis, the causative agent of the disease tuberculosis (TB). Among these exposed individuals, 5-10% develop active TB over the course of their lifetime. Improved socioeconomic conditions, general health and the use of effective antimicrobial drug treatment have resulted in reduced exposure and a decrease in disease rates in many geographic regions. In other areas of the world, however, the public health measures required to adequately control TB are not optimal, making this disease a significant source of mortality and morbidity.
Members of the IL12 family of cytokines have been demonstrated to be important for immune-mediated control of M. tuberculosis. The research objectives of my laboratory include (1) testing what cell types must respond to IL12 family members in order to both control M. tuberculosis infection and limit TB-associated lung pathology and (2) characterizing endogenously expressed IL12 receptor agonists/antagonists. To meet these objectives we use a mouse model of TB that recapitulates important aspects of the human disease. Specifically, the model involves a low-dose (~75-100CFU) aerogenic infection of inbred mice with the virulent M. tuberculosis strain H37Rv. In order to assess the importance of select genes to control infection, my lab utilizes, in addition to wild type mice, both gene-knockout (KO) and transgenic (Tg) strains of mice on the same genetic background. Any difference observed between wild type and KO/Tg animals (in terms of either their control of bacterial burden or immune response to the pathogen) provides insight into how an individual gene regulates disease.
It is the goal of the Robinson lab that the data from our experiments not only influences scientists’ understanding of human infection with M. tuberculosis, but also the identification of cell lineages and proteins in the lung whose modification may improve TB control and treatment.
Shown is an acid fast stain of Mtb-infected lungs from IL12-deficient mice. Although lymphocytes are present in the lung and localize near infected phagocytes, since IL12 is absent lymphocytes only have a limited ability to protect the host.
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