Institute for Metabolism and Immunology

(Formerly known as TDI - Type 1 Diabetes Immunology)
Our overarching goal is to understand how the immune system interacts with metabolic processes in health and disease, and how this interplay can be harnessed for precision prevention and therapies. A central focus is on regulatory T cells (Tregs), key players in immune-metabolic crosstalk. We have a longstanding interest in autoimmune type 1 diabetes as a paradigm to study how immune regulation shapes metabolic outcomes. We aim to uncover how Treg specialization and dysfunction contribute to metabolic diseases such as diabetes and how these insights can guide targeted interventions. Our vision is to develop strategies that not only modulate immune responses but also support tissue function, regeneration, and repair. Ultimately, we seek to translate mechanistic insights into disease-specific interventions that improve metabolic health and prevent complications.

(Formerly known as TDI - Type 1 Diabetes Immunology)

Our overarching goal is to understand how the immune system interacts with metabolic processes in health and disease, and how this interplay can be harnessed for precision prevention and therapies. A central focus is on regulatory T cells (Tregs), key players in immune-metabolic crosstalk. We have a longstanding interest in autoimmune type 1 diabetes as a paradigm to study how immune regulation shapes metabolic outcomes. We aim to uncover how Treg specialization and dysfunction contribute to metabolic diseases such as diabetes and how these insights can guide targeted interventions. Our vision is to develop strategies that not only modulate immune responses but also support tissue function, regeneration, and repair. Ultimately, we seek to translate mechanistic insights into disease-specific interventions that improve metabolic health and prevent complications.

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Regulatory T cells (Tregs) are key players in maintaining peripheral immune tolerance. Beyond their classical role, recent research, including our own, has revealed that Tregs also shape metabolic tissue integrity, function and regeneration, thereby influencing systemic metabolism. By studying both the classical functions of Tregs and their role in immune-metabolic tissue crosstalk, the Institute for Metabolism and Immunology investigates the central drivers of metabolic health. Our research aims include dissecting Treg specialization in metabolic disease, understanding Treg – metabolic tissue crosstalk, developing translational models to target Tregs, and ultimately designing Treg modulators to prevent or treat metabolic diseases.

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A joint study by Helmholtz Munich, the German Center for Diabetes Research (DZD), and Goethe University Frankfurt reveals how a novel drug may help prevent type 1 diabetes (T1D) by restoring immune balance. The findings were published in Molecular…

3D representation of insulin protein structure illuminated with a blue glow on a black background_AdobeStock_1073210391

At this year’s Congress of the German Diabetes Association (DDG), three researchers from Helmholtz Munich were honored for their outstanding scientific achievements. Their groundbreaking work is helping to advance the understanding, prevention, and…

A study led by researchers from Helmholtz Munich and the German Center for Diabetes Research (DZD) unveils a key communication pathway between the immune system and metabolism in the hypothalamic region of the brain. By identifying the role of…

Every year on October 3rd, the German broadcaster WDR organizes the event "Doors Open with The Mouse." This year, 770 companies and research institutions across Germany participated, welcoming children and parents under the theme "Working Together."…

A recent discovery led by Helmholtz Munich researchers from the Type 1 Diabetes Immunology Research Unit has uncovered how regulatory immune T-cells (called Tregs) interplay and control metabolic tissues. The new findings published in Cell…

How do our muscles respond at the molecular level to exercise? Researchers at Helmholtz Munich and the German Institute of Human Nutrition Potsdam-Rehbrücke (DIfE) have unraveled the cellular basis and signaling pathways responsible for the positive…

Helmholtz Munich researchers receive 2.25 Mio US Dollar JDRF Grant

With a 2.25 million US dollar grant provided by the Juvenile Diabetes Research Foundation (JDRF), Prof. Matthias Hebrok, Prof. Heiko Lickert, and Prof. Carolin Daniel from the…

Prof. Carolin Daniel

IMI Director

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Dr. Isabelle Serr

Deputy Head

Dr. Maike Becker

Deputy Head

Dr. Martin Scherm

Scientific Affairs Lead

Laura Harrison

Scientific Coordinator

Maria Rocha Acevedo

Scientific Coordinator

Franziska Schadl

Biology Lab Technician

Michael Lauber

Bioinformatics Specialist

Sandra Maria Kydd

Postdoc

Dr. Camilla Tondello

Postdoc

Anne Helena Neubig

Doctoral Researcher

Till Johannsmann

Doctoral Researcher

Gianmarco Spata

Doctoral Researcher

Emily Schardey

Doctoral Researcher

Anne-Marie Bührer

Doctoral Researcher

Anna Kovordànyi

Student Assistant

Khushboo Garg

Student Assistant

Hipp H, Tondello C, Gmehling H, Scholz LK, Stavridou A, Becker M, Bührer A-M, Hintermann E, Dirschl SM, Johannsmann TM, Scherm MG, Kohlhof H, Serr I, Christen U, Daniel C

Inhibition of pyrimidine de novo synthesis fosters Treg cells and reduces diabetes development in models of Type 1 Diabetes

Becker M, Kälin S, Neubig AH, Lauber M, Opaleva D, Hipp H, Salb VK, Ott VB, Legutko B, Kälin RE, Hippich M, Scherm MG, Nascimento LFR, Serr I, Hosp F, Nikolaev A, Mohebiany A, Krueger M, Flachmeyer B, Pfaffl MW, Haase B, Yi C-X, Dietzen S, Bopp T, Woods SC, Waisman A, Weigmann B, Mann M, Tschöp MH, Daniel C

Regulatory T cells in the mouse hypothalamus control immune activation and ameliorate metabolic impairments in high-calorie environments

Becker M, Joseph S, Garcia-Carrizo F, Tom R, Opaleva D, Serr I, Tschöp M, Schulz T, Hofmann S, Daniel C

Regulatory T cells require IL6 receptor alpha signaling to control skeletal muscle function and regeneration

Scherm MG, Serr I, Zahm AM, Schug J, Bellusci S, Manfredini R, Salb VK, Gerlach K, Weigmann B, Ziegler AG, Kaestner KH, Daniel C

miRNA142-3p targets Tet2 and impairs Treg differentiation and stability in models of type 1 diabetes

Becker M, Serr I, Salb VK, Ott VB, Mengel L, Blüher M, Weigmann B, Hauner H, Tschöp MH, Daniel C.

Short-term cold exposure supports human Treg induction in vivo

Serr I, Scherm MG, Zahm AM, Schug J, Flynn VK, Hippich M, Kälin S, Becker M, Achenbach P, Nikolaev A, Gerlach K, Liebsch N, Loretz B, Lehr C-M, Kirchner B, Spornraft M, Haase B, Segars J, Küper C, Palmisano R, Waisman A, Willis RA, Kim W-U, Weigmann B, Kaestner KH, Ziegler AG, Daniel C.

miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes

Kälin S, Becker M, Ott VB, Serr I, Hosp F, Mollah MMH, Keipert S, Lamp D, Rohner-Jeanrenaud F, Flynn VK, Scherm MG, Nascimento LFR, Gerlach K, Popp V, Dietzen S, Bopp T, Krishnamurthy P, Kaplan MH, Serrano M, Woods SC, Tripal P, Palmisano R, Jastroch M, Bluher M, Wolfrum C, Weigmann B, Ziegler AG, Mann M, Tschöp MH, Daniel C.

A Stat6/Pten Axis Links Regulatory T Cells with Adipose Tissue Function

Serr I, Fürst RW, Ott VB, Scherm MG, Nikolaev A, Gökmen F, Kälin S, Zillmer S, Bunk M, Weigmann B, Kunschke N, Loretz B, Lehr CM, Kirchner B, Haase B, Pfaffl MW, Waisman A, Willis RA, Ziegler AG, Daniel C

miRNA92a taargets KLF2 and PTEN signaling to promote human T follicular helper precursors in T1D islet autoimmunity

Serr I, Fürst RW, Achenbach P, Scherm MG, Gökmen F, Haupt F, Sedlmeier E-M, Knopff A, Shultz L, Willis RA, Ziegler A-G, Daniel C.

Type 1 diabetes vaccine candidates promote human Foxp3+Treg induction in humanized mice

Daniel C, Weigmann B, Bronson R, von Boehmer H

Prevention of type 1 diabetes in mice by tolerogenic vaccination with a strong agonist insulin mimetope

Daniel C, Wennhold K, Kim HJ, von Boehmer H

Enhancement of antigen-specific Treg-vaccination in vivo

Nolting J, Daniel C, Reuter S, Stuelten C, Li P, Sucov H, Kim BG, Letterio JJ, Kretschmer K, Kim HJ, von Boehmer H

Retinoic acid can enhance conversion of naive into regulatory T cells independently of secreted cytokines