Skip to Main Content

Martin Kriegel, MD, PhD

Associate Professor Adjunct
DownloadHi-Res Photo

About

Titles

Associate Professor Adjunct

Biography

Dr. Kriegel is currently Chief of Rheumatology and Clinical Immunology at the University of Münster, Germany, while remaining an Associate Professor Adjunct of Immunobiology and of Medicine (Rheumatology) at Yale School of Medicine. In 2001, he received his MD/PhD equivalent at the Friedrich-Alexander University of Erlangen, Germany, followed by the German Medical Licensure in 2002. From 2003 to 2006, he performed postdoctoral training in the Flavell lab at Yale. From 2006 to 2012, he completed a medicine residency and rheumatology fellowship at Beth Israel Deaconess Medical Center and Brigham & Women’s Hospital, Boston, as well as additional research in the Benoist/Mathis laboratory at Harvard Medical School. Dr. Kriegel returned to Yale in 2012 as an Assistant Professor in the Department of Immunobiology and an Attending Physician in Rheumatology at Yale-New Haven Hospital. In 2017, Dr. Kriegel became a Senior Principal Scientist at Roche, and in 2020, he took a position as Chair of Translational Rheumatology and Immunology at the University of Münster, Germany, while maintaining his adjunct faculty position at Yale with ongoing collaborations within the Department of Immunobiology.

Appointments

Education & Training

Rheumatology Fellowship
Brigham and Women's Hospital, Harvard Medical School (2012)
Residency
Beth Israel Deaconess Medical Center, Harvard Medical School (2008)
Postdoctoral Fellowship
Yale University School of Medicine (2006)
Clinical Fellowship
University Hospital, Erlangen, Germany (2003)
PhD
Friedrich-Alexander University of Erlangen-Nurn (2001)
MD
Friedrich-Alexander University of Erlangen (2000)

Research

Overview

The Kriegel lab has moved to Münster, Germany (University of Münster), where the following research is being continued besides ongoing collaborations with investigators at Yale:

We are broadly interested in the role of commensal organisms in the development of autoimmunity. A major question in the lab is whether an autoimmune-prone host that is persistently colonized with cross-reactive commensals, develops chronic autoimmunity via molecular mimicry. We address this hypothesis using the antiphospholipid syndrome as a model disease since the structure and antigenic epitopes are well characterized for the major autoantigen and infectious triggers have been implicated in the pathogenesis. We are also exploring whether prokaryotic commensal protein orthologs can trigger autoreactivity in systemic lupus erythematosus. We study both human samples in vitro and autoimmune murine models in vivo.

In this context, we have characterized the commensal- and autoepitope-specific CD4+ T and B cell responses using synthetic peptides, recombinant fusion proteins as well as protein extracts from cultured anaerobic commensal candidates. We are further applying 16S rRNA-based realtime PCR and next-generation sequencing approaches in order to identify novel candidates. The mouse models we use include the lupus-prone (NZWxBXSB)F1 hybrid and Toll-like receptor 7 transgenic mice. We simultaneously study two knock-out mouse models of autoimmunity that we have crossed to the lupus-prone strains. We plan to merge both human and mouse studies in humanized, gnotobiotic animals that are colonized with human microbiota.

Another research avenue is the effect of genetic variants of the host immune system on the composition and function of the gut microbiome. We are exploring a particular autoimmunity-predisposing single nucleotide polymorphism and its impact on gut microbial community structures. Similar approaches as above will be employed to dissect the host-microbe interactions under the influence of genetic variants.

A third interest in the lab is the impact of dietary components on the autoimmune gut microbiome. We are actively pursuing studies that address the potential protective effects of certain diets in lupus- and antiphospholipid syndrome-prone mouse models. We aim to elucidate the contribution of the gut microbiota and differentiate it from direct host effects. These efforts should lead to the development of more selective therapeutic avenues that are targeting specifically the gut microbiota.

Lastly, we are studying endogenous retroviruses and their interactions with the gut microbiota in systemic autoimmunity. We use RT-PCR-based strategies to detect and quantify endogenous retroviruses in various contexts and couple these studies with microbiome research detailed above.

In summary, the overarching goal of our research is to discover causal factors within the gut microbiomes of autoimmune-prone individuals, to better understand gut microbial interactions with the host and environmental components, and to manipulate gut microbial communities as a novel therapeutic approach in autoimmunity.

Medical Subject Headings (MeSH)

Autoimmunity; Bacteria; Host-Pathogen Interactions; Immune System Diseases; Immune Tolerance; Immunity, Mucosal; Lymphocyte Activation

Research at a Glance

Yale Co-Authors

Frequent collaborators of Martin Kriegel's published research.

Publications

Featured Publications

2024

2023

2022

Academic Achievements & Community Involvement

  • activity

    Current Opinion in Structural Biology

  • honor

    Global Team Science Award

  • activity

    National Institutes of Health

  • honor

    Lupus Insight Prize

  • activity

    Chair of Rheumatology and Clinical Immunology

Get In Touch