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Janis Weis, Ph.D.

last modified 2008-07-08 11:31 — by u0189572

Professor of Pathology

Scholarly Emphasis: Lyme Arthritis
Janis Weis, Ph.D.

Janis Weis, Ph.D.

Contact Info

Email Address: janis.weis |@| path.utah.edu

Office Phone Number: 801.581.8386

Location: 1720 Emma Eccles Jones Medical Research Building

Research Lab: Janis Weis' Lab

Division: Cell Biology & Immunology

Also Works in: Microbial Pathogenesis  

 

About Janis Weis, Ph.D.

Microbial Pathogenesis Seminar Series

The Microbial Pathogenesis Seminar Series provides a forum for outstanding presentations in the disciplines of Microbiology, Virology, Immunology, and Host-pathogen interactions.  Speakers are selected from within the University of Utah or are invited from outside institutions, and presentations are given on the 2nd and 4th Fridays of the month at noon.  Participants are from several departments encompassing both the basic sciences and clinical departments, with the interchange among those with clinical perspective and research perspective being one of the intended goals.  Departments that regularly participate in this series include Pathology, Biochemistry, Medicine, Pediatrics, Biology, and Medicinal Chemistry.  The MPSS receives support from the Microbial Pathogenesis Training Grant, the Weber Trust in Immunology, the Vice President for Health Sciences, and Myriad Genetics.

 Microbial Pathogenesis Training Grant

The Microbial Pathogenesis Training Grant is funded by the National Institute of Allergy and Immunology of the NIH, and supports 3 pre-doctoral and 3 post-doctoral trainees working on projects in the area of microbial pathogenesis.  Trainees are involved in hosting and meeting seminar speakers through the Microbial Pathogenesis Seminar Series, take courses in Microbial Pathogenesis and Immunology, participate in a journal club in Microbial Pathogenesis, and present their research at an annual retreat.  An outstanding caliber of research is expected and achieved by trainees of the Microbial Pathogenesis Training Grant.

Selected Publications

  • Ribeiro JMC., Weis JJ, Telford SR. Saliva of the tick Ixodes dammini inhibits neutrophil function. Exp Parasitol. 1990; 70:382-388.
  • Schoenfeld R, Araneo B, Ma Y, Yang L,Weis JJ. Demonstration of a B-lymphocyte mitogen produced by the Lyme disease pathogen, Borrelia burgdorferi Infect. Immun. 1992 60:455-64.
  • Yang L, Ma Y, Schoenfeld R, Griffiths M, Eichwald E, Araneo B, Weis JJ. Evidence for B lymphocyte mitogen activity in Borrelia burgdorferi infected mice. 1992 Infect. Immun. 60:3033-3041.
  • Ma Y and Weis JJ. Borrelia burgdorferi outer surface lipoproteins OspA and OspB possess B cell mitogen and cytokine stimulatory properties. 1993 Infect. Immun. 61:3842-3853.
  • Yang L, Weis JH, Eichwald E, Kolbert CP, Persing D. and Weis JJ. Heritable susceptibility to Borrelia burgdorferi induced arthritis is dominant and is associated with persistence of high numbers of spirochetes in tissues. 1994. Infect.Immun., 62:491-500.
  • Wooten RM, Modur VJ, McIntyre TM, Weis JJ. Borrelia burgdorferi outer membrane protein A induces nuclear translocation of NF-b and inflammatory activation in human endothelial cells 1996. J. Immunol.. 157:4584-4590.
  • Morrison TB, Weis JH, Weis JJ. Borrelia burgdorferi outer surface protein A (OspA) activates and primes human neutrophils. 1997. J. Immunol., 158:4838-4845
  • Ma Y, Seiler KP, Eichwald EJ, Weis JH, Teuscher C, Weis JJ. Distinct characteristics of resistance to Borrelia burgdorferi-induced arthritis in C57BL/6N mice. 1998 Infect.Immun. 66:161-8
  • Wooten RM, Morrison TB, Weis JH, Wright SD, Thieringer R, Weis JJ. The role of CD14 in signaling mediated by outer membrane lipoproteins of Borrelia burgdorferi. 1998. J. Immunol. 160:5485-5492
  • Morrison, TB, Weis, JJ, Wittwer, CT. Quantification of low copy transcripts by continuous SYBR Green I monitoring during amplification. 1998. Biotechniques 24 (No 6): 954-959.
  • Seiler KP, Ma Y, Weis JH, Frenette PS, Hynes RO, Wagner DD, Weis JJ. E- and P-Selectin are not required for resistance to severe murine Lyme arthritis. 1998 Infect. Immun. 66:4457-9.
  • Weis JJ, McCracken BA, Ma Y, Fairburn D, Weis JH, Roper, R, Morrison TB, Zachery JF, Doerge RW, Teuscher C. Identification of quantitative trait loci governing arthritis severity and humoral responses in the murine model of Lyme disease. 1999 J. Immunol. 162:948-956.
  • Morrison TB, Ma Y, Weis JH, Weis JJ. Rapid and sensitive quantification of Borrelia burgdorferi -infected mouse tissues using continuous fluorescent monitoring of PCR. 1999 J. Clin Micro. 37:987-992.
  • Brown JP, Zachary JF, Teuscher C, Weis JJ, Wooten RM. Dual role of IL-10 in murine Lyme disease: regulation of arthritis severity and host defense. 1999 Infect. Immun. 67:5142-5150.
  • Hirschfeld M, Kirschning CJ, Schwandner R, Wesche H, Weis JH, Wooten RM, and Weis JJ. Inflammatory signaling by Borrelia burgdorferi lipoproteins is mediated by toll-like receptor 2. 1999 J. Immunol. 163:2382-2386.
  • Hirschfeld M, Ma Y, Weis JH, Vogel SN, Weis JJ. Repurification of LPS eliminates signaling through both human and murine Toll-like receptor 2. 2000. J.Immunol. 165:618-622.
  • Potter MR, Noben-Trauth N, Weis, JH, Teuscher C, Weis JJ. Interleukin-4 (IL-4) and IL-13 signaling pathways do not regulate Borrelia burgdoferi-induced arthritis in mice: IgG1 is not required for host control of tissue spirochetes. 2000. Infect. Immun. 68:5603-5609.
  • Hirschfeld M, Weis JJ, Toshchakov V, Salkowski CA, Cody MJ, Ward DC, Qureshi N, Michalek SM, Vogel SN. Signaling by Toll-Like receptor 2 and 4 agonists results in differential gene expression in murine macrophages. 2001 Infect. Immun. 69:1477-1482.
  • Wooten RM, Weis JJ. Host-pathogen interactions promoting inflammatory Lyme arthritis: Use of mouse models for dissection of disease processes. 2001. Current Opinion in Microbiology. 4:274-279.
  • Roper R.J., 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. 2001 . Genes and Immunity. 2:388-397.
  • Wooten RM, Ma Y, Yoder RA, Brown JP, Weis JH, Zachary JF, Kirschning CJ. Weis JJ. Toll-like receptor 2 is required for innate but not acquired host defense to Borrelia burgdorferi. 2002. J. Immunol 168:358-355.
  • Potter MR, Rittling SR, Denhardt DT, Roper RJ, Weis J, Teuscher C, Weis JJ. Role of osteopontin in murine Lyme arthritis and host defense to Borrelia burgdorferi. 2002. Infect. Immun 70:1372-1381.
  • Weis, JJ. Host-pathogen interactions and the pathogenesis of murine Lyme disease. 2002 Current Opinion in Rheumatology. 14:399-403.
  • Lawrenz MB, Wooten RM, Zachary JF, Drouin SM, Weis JJ, Wetsel, RA, Norris SJ. Effect of complement component C3 deficiency on experimental Lyme borreliosis in mice. 2003 Infect. Immun. 71: 4432-4440
  • Yoder A, Wang X, Ma Y, Philipp MT, Heilbrun M, Weis JH, Kirschning CJ, Wooten RM, Weis JJ. Pam3Cys-dependent OspA-vaccination of TLR2-deficient mice results in effective protection from B. burgdorferi challenge. 2003., Infect. Immun.71:3894-3900
  • Wooten RM, Ma Y, YoderRA, Brown JP, Weis JH, Zachary JF, Kirschning CJ, Weis JJ. Toll-like receptor 2 plays a pivotal role in host defense and inflammatory response to Borrelia burgdorferi. 2002. Vector Borne and Zoonotic Diseases. 2:275-278.
  • Bolz DD, Weis JJ. Molecular Mimicry to Borrelia burgdorferi: Pathway to Autoimmunity? 2004 Autoimmunity. 37:387-392
  • Wang G, Ma Y, Buyuk A, McClain S, Weis JJ, Schwartz I. Impaired host defense to infection and Toll-like receptor 2-independent killing of Borrelia burgdorferi clinical isolates in TLR2-deficient C3H/HeJ mice. 2004. FEMS Microbiol Lett. 231:219-225.
  • Bolz, D.D., Sundsbak, R.S., Ma, Y., Akira, S., Kirschning, C.J., Zachary, J.F., Weis, J.H., Weis, J.J. MyD88 plays a unique role in host defense but not arthritis development in Lyme Disease. 2004. J. Immunol. 173:2030-2010.
  • Wang X, Ma Y, Weis JH, ZacharyJF, Kirschning, CJ, Weis JJ. Relative contributions of innate and acquired host responses to bacterial control and arthritis development in Lyme disease. 2005 Infect. Immun. 73:657-660
  • Crandall H, Ma Y, Dunn DM, Sundsbak RS, Holmdahl R, Olofsson P, Zachary JF, Weis JH, Weiss RB, Teuscher C, Weis JJ. Bb2Bb3 regulation of murine Lyme arthritis is distinct from Ncf1 and independent of the phagocyte NADPH oxidase. 2005 American Journal of Pathology 167:775-785.
  • Stewart PE, Wang X, Bueschel DM, Clifton DR, Grimm D, Tilly K, Carroll JA, Weis JJ, Rosa PA. 2006. Delineating the requirement for the Borrelia burgdorferi virulence factor OspC in the mammalian host. Infect Immun 74:3547-3553.
  • Bolz, DD, Sundsbak RS, Ma Y, Akira S, Weis JH,. Schwan TG, Weis JJ. Dual Role of MyD88 in Rapid Clearance of Relapsing Fever Borrelia 2006, Infect. Immun. 74:6750-6760.
  • Crandall H, Dunn DD, Ma Y, Wooten RM, Zachary JF, Weis JH, Weiss RB, Weis JJ. Gene Expression Profiling Reveals Unique Pathways Associated with Differential Severity of Lyme Arthritis. 2006 J. Immunol. 177:7930-42.
  • All Publications: Click Here

Honors and Awards

  • 3rd recipient of the C. Scott and Dorothy E. Watkins Endowed Chair honoring Ernst J. Eichwald, M.D