Dr. Teuscher received his Ph.D. in Pathology at the University of New Mexico in 1982. In 1984 he joined the faculty at the University f Pennsylvania School of Medicine. Dr. Teuscher returned to the Intermountain West as an Associate Professor of Microbiology at Brigham Young University. In 2001, following a stent at the University of Illinois Urbana-Champaign as a Professor of Veterinary Pathobiology, he moved to the University of Vermont where he is a Professor of Medicine and Pathology.

Research Interests

A co-evolutionary genetic link between susceptibility to infectious and autoimmune disease has long been suspected. In the molecular arms race between pathogens and host defense genes, polymorphism in genes controlling antigen-specific molecular interactions are considered the quintessential examples of infectious disease gene alleles that contribute to autoimmune disease susceptibility. However, it has been estimated that approximately half of the host genetic variability contributing to infectious disease resistance is a function of genes encoding for non-antigen specific molecules. Thus, the identification of polymorphic, non-antigen dependent molecules controlling susceptibility to infectious agents, or their products, and autoimmune disease would provide considerable insight into the nature of such genes. With the advent of genome scanning technology and high resolution congenic mapping, a large number of infectious and autoimmune disease susceptibility loci have been mapped. Early on it became evident that several of these loci resided on the same chromosomes and colocalized within the same genetic intervals. We hypothesized that this phenomenon represented either single, shared disease susceptibility genes or members of gene complexes involved in multiple immunopathologically mediated phenotypes. This hypothesis has recently been validated when we identified Bphs, the locus controlling susceptibility to Bordetella pertussis induced hypersensitivity to histamine and autoimmune disease in mice, as the histamine H1 receptor. Mechanistically, Bphs/Hrh1 controls both the induction and effector phases of the disease process. Similar positional-candidate gene cloning approaches are underway to identify genes underlying previously mapped infectious and autoimmune disease QTL in the mouse.

Selected Publications

Teuscher C, Bunn JY, Fillmore PD, Butterfield RJ, Zachary JF, Blankenhorn EP. Gender, age, and season at immunization uniquely influence the genetic control of susceptibility to histopathological lesions and clinical signs of experimental allergic encephalomyelitis: implications for the genetics of multiple sclerosis. Am J Pathol. 2004, 165:1593-602.

Teuscher C, Poynter ME, Offner H, Zamora A, Watanabe T, Fillmore PD, Zachary JF, Blankenhorn EP. Attenuation of Th1 effector cell responses and susceptibility to experimental allergic encephalomyelitis in histamine H2 receptor knockout mice is due to dysregulation of cytokine production by antigen-presenting cells. Am J Pathol. 2004, 164:883-92.

McAllister RD, Singh Y, du Bois WD, Potter M, Boehm T, Meeker ND, Fillmore PD, Anderson LM, Poynter ME, Teuscher C. Susceptibility to anthrax lethal toxin is controlled by three linked quantitative trait loci. Am J Pathol. 2003, 163:1735-41.

Roper RJ, McAllister RD, Biggins JE, Michael SD, Min SH, Tung KS, Call SB, Gao J, Teuscher C. Aod1 controlling day 3 thymectomy-induced autoimmune ovarian dysgenesis in mice encompasses two linked quantitative trait loci with opposing allelic effects on disease susceptibility. J Immunol. 2003, 170:5886-91.

Butterfield RJ, Roper RJ, Rhein DM, Melvold RW, Haynes L, Ma RZ, Doerge RW, Teuscher C. Sex-specific quantitative trait loci govern susceptibility to Theilers murine encephalomyelitis virus-induced demyelination. Genetics 2003, 163:1041-6.

Ma RZ, Gao J, Meeker ND, Fillmore PD, Tung KS, Watanabe T, Zachary JF, Offner H, Blankenhorn EP, Teuscher C. Identification of Bphs, an autoimmune disease locus, as histamine receptor H1. Science 2002, 297:620-3.

Roper RJ, Weis JJ, McCracken BA, Green CB, Ma Y, Weber KS, Fairbairn D, Butterfield RJ, Potter MR, Zachary JF, Doerge RW, Teuscher C. Genetic control of susceptibility to experimental Lyme arthritis is polygenic and exhibits consistent linkage to multiple loci on chromosome 5 in four independent mouse crosses. Genes Immun. 2001, 2:388-97.

CMB Lab Members