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Reinhard Hinterleitner Ph.D.

  • Assistant Professor, Department of Immunology
  • PMI Graduate Faculty

    Education & Training

  • University of Chicago, Postdoc
  • Medical University Innsbruck – Austria, Ph.D. (2012)
  • University of Applied Sciences Vienna – Austria, M.S. (2007)
Representative Publications

Sangani KA, Parker ME, Anderson HD, Chen L, Pandey SP, Pierre JF, Meisel M, Riesenfeld SJ, Hinterleitner R, Jabri B. Epigenetic control of commensal induced Th2 responses and intestinal immunopathology. bioRxiv  [Preprint]. 2024 Aug 30:2024.08.30.610485.  PMID: 39257820

Galipeau HJ, Hinterleitner R, Leonard MM, Caminero A. Non-host factors influencing onset and severity of celiac disease. Gastroenterology 2024 Jan 27:S0016-5085(24)00068-4. PMID: 38286392

Fiske K, Brigleb PH, Medina Sanchez L, Hinterleitner R, Taylor GM, Dermody TS. Stain-specific differences in reovirus infection of murine macrophages segregate with polymorphisms in viral outer-capsid protein s3. Journal of Virology 2024 Oct 21:e0114724. PMID: 39431846

Medina Sanchez L#, Siller M#, Zeng Y#, Brigleb PH, Sangani KA, Soto AS, Engl C, Laughlin CR, Rana M, Van Der Kraak L, Pandey SP, Bender MJ, Fitzgerald B, Hedden L, Fiske K, Taylor GM, Wright AP, Mehta ID, Rahman SA, Galipeau HJ, Mullett SJ, Gelhaus SL, Watkins SC, Bercik P, Nice TJ, Jabri B, Meisel M, Das J, Dermody TS, Verdú EF, Hinterleitner R. The gut protist Tritrichomonas arnold restrains virus-mediated loss of oral tolerance by modulating dietary antigen-presenting dendritic cells. Immunity 2023 Jul 11;S1074-7613(23)00279-0. # contributed equally.

Bender MJ#, McPherson AC#, Phelps CM, Pandey SP, Laughlin CR, Shapira JK, Medina Sanchez L, Rana M, Richie TG, Mims TS, Gotcher-Demske AM, Cervantes-Barragan L, Mullett SJ, Gelhaus SL, Bruno TC, Cannon N, McCulloch JA, Vignali DAA, Hinterleitner R, Joglekar AV, Pierre JF, Lee STM, Davor D, , Zarour HM, Meisel M. Dietary tryptophan metabolite released by intratumoral Lactobacillus reuteri facilitates immune checkpoint inhibitor therapy. Cell 2023 Apr 4:S0092-8674(23)00271-4. # contributed equally. PMID: 37028428

Brigleb PH, Kouame E, Fiske K, Taylor GM, Urbanek K, Medina Sanchez L, Hinterleitner R, Jabri B#, Dermody TS#. Natural killer cells contribute to reovirus-induced interferon responses and loss of tolerance to dietary antigen. JCI Insight 2022 Aug 22;7(16):e159823. # contributed equally. PMID: 35993365

Pandey SP, Bender MJ, McPherson AC, Phelps CM, Medina Sanchez L, Rana M, Hedden L, Sangani KA, Chen L, Shapira JH, Siller M, Goel C, Verdú EF, Jabri B, Chang A, Chandran UR, Mullett SJ, Wendell SG, Singhi AD, Tilstra JS, Pierre JF, Arteel GE, Hinterleitner R, Meisel M. Tet2 deficiency drives liver microbiome dysbiosis triggering Tc1 cell autoimmune hepatitis. Cell Host & Microbe 2022 May 27:S1931-3128(22)00266-9. PMID: 35658976

Siller M#, Zeng Y#, Hinterleitner R. Can microbes boost Tregs to suppress food sensitivities? Trends in Immunology 2020 Oct 6:S1471-4906(20)30212-X. # contributed equally. PMID: 33036909

Hinterleitner R#, Meisel M#, Pacis A, Chen L, Earley ZM, Mayassi T, Pierre JF, Ernest JD, Galipeau HJ, Thuille N, Bouziat R, Buscarlet M, Ringus DL, Wang Y, Li Y, Dinh V, Kim SM, McDonald BD, Zurenski MA, Musch MW, Furtado G, Lira S, Baier G, Chang EB, Eren MA, Weber CR, Busque L, Godley LA, Verdú EF, Barreiro LB, Jabri B. Microbial signals drive pre-leukaemic myeloproliferation in a Tet2-deficient host. Nature 2018 May;557(7706):580-584. # contributed equally. PMID: 29769727

Hinterleitner R#, Bouziat R#, Brown JJ#, Stencel-Baerenwald JE, Ikizler M, Mayassi T, MeiselM, Kim SM, Discepolo V, PruijssersAJ, ErnestJD, IskarpatyotiJA, CostesLMM, Lawrence I, Palanski BA, Varma M,ZurenskiMA, Khomandiak S, McAllister N, AravamudhanP, BoehmeKW, Hu F, Samsom JN, Reinecker HC, Kupfer SS, Guandalini S, Semrad C, Abadie V, Khosla C, Barreiro LB, Xavier RJ, Ng A, Dermody TS, Jabri B. Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease. Science 2017 Apr 7;356(6333):44-5 #contributed equally. PMID:  28386004

Complete list of publications

Research Interests

IDENTIFY TRIGGERS THAT LEAD TO ABERRANT TYPE 2 IMMUNE-MEDIATED FOOD ALLERGIES

We have shown that enteric reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease (Science, 2017). Loss of oral tolerance to gluten antigen is characterized by proinflammatory T-helper 1 immune responses. However, in contrast to celiac disease, classical food allergies such as peanut allergy for example are initiated via T-helper 2 immune responses going wrong. One aim of my lab is to study and identify triggers that lead to aberrant T-helper 2 immune-mediated food allergies using genetically engineered mouse models, various immunological tools and by collaborating with the food allergy program at the University of Pittsburgh allowing us to translate our findings to human health.
IMPACT OF SOMATIC MUTATIONS ON INTESTINAL BARRIER INTEGRITY

Age-acquired somatic TET2 mutations increase the risk for hematopoietic malignancies. We have shown that microbial signals drive pre-leukemic myeloproliferation in a Tet2-deficient host (Nature, 2018), suggesting new ways of preventing disease development. In this study we have identified that defects in the small intestinal gut barrier lead to systemic bacteria translocation resulting in pre-leukemic myeloproliferation. One aim of my lab is to define the underlying mechanism of this gut barrier defect and to identify potential intestinal abnormalities in humans with somatic TET2 mutations.
INTESTINAL GENE MACHINE

From the very proximal part of the intestine, which is the duodenum, to the very distal part of the colon, this entire organ has highly-specialized site-specific functions and is characterized by differences in the composition of intestinal microbes and host immune cells residing in the epithelium and lamina propria. With the use of next generation sequencing we have identified site-specific genes and want to define their function and relevance under homeostasis and presence of inflammatory triggers using CRISPR-engineered genetically modified mice, organoid co-cultures and various molecular techniques

The Hinterleitner lab is currently accepting graduate students for rotations in the laboratory, as well as applications for postdoctoral fellows.