Assistant Professor 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.
DCs express an IL12Rβ1 alternative splice variant following exposure to M. tuberculosis. (A) The genomic position and organization of the murine il12rb1 locus. Exons 1-16 are denoted e.1-e.16. Upon transcription and intron-removal (B) e.1-13 become the extracellular-encoding (EC) portion of the IL12Rβ1 transcript, e.14 the transmembrane-encoding (TM) portion, and e15-16 the intracellular-encoding (IC) portion. Shown to the right of the transcript are the relative positions of primers 1-5 (P1-P5; down triangle indicates a forward primer and up triangle indicates a reverse primer) used for (C) amplification of IL12Rβ1 cDNA from the indicated cell populations. (D-E) Sequencing of the smaller amplicon of P3-P5 (indicated by arrow) reveals an IL12Rβ1 alternative splice variant that contains both a 97bp deletion and (E) a frameshift insertion that eventually produces a premature stop codon.
Recent Publications
Contact Information
Email: rrobinson@mcw.edu Phone: 414-955-2976 Room: BSB 256