Hermann Wagner (born May 20, 1941) is a German scientist in the field of microbiology and immunology and past Dean of the Medical Faculty of the Technical University Munich (TUM). His massive number of published works, at over 370, makes him one of Europe's most cited immunologists. [1]
Wagner studied Medicine and in 1967 received his medical degree (MD) from the University of Tübingen.[ citation needed ] In Melbourne, Australia he studied Human Biology and in 1973 received his PhD from University of Melbourne.[ citation needed ] From 1973 to 1983 he continued his research on "T Cell mediated Immune Responses" with Paul Klein at the Institut of Microbiology of the Johannes-Gutenberg University in Mainz, Germany.[ citation needed ] In 1978, he qualified as a university lecturer (habilitation), and in 1983 he was made full professor and head of the Institut of Microbiology at the University of Ulm.[ citation needed ] In 1989 he moved to the Technical University Munich, where he headed the Institute of Medical Microbiology, Immunology and Hygiene. [2] [3] He retired at the end of 2008.[ citation needed ]
His prime research activities focus on mechanisms of protective immunity towards pathogens. [3] From 1970-80 he analysed T-T Cell interactions during the induction of cytotoxic T Cell responses. [4] During his Ulm period he focussed on the immunobiology of bacterial superantigens. [5] In Munich, he subsequently contributed to our understanding of Toll-like-Receptors(TLR), through which innate immune cells sense pathogens. In particular he was one of the first to realise [6] that bacterial/viral DNA activated Innate Immune cells via TLR9.[ citation needed ] Conversely his group was able to show that TLR7 and/or TLR8 recognised pathogen-derived RNA [2] [7] while TLR13 senses bacterial 23S rRNA. [8]
In Ulm he initiated and headed the Collaborative Research Program of the German Research Council (Sonderforschungsbereich) entitled "Lympo-Haemopoese".[ citation needed ] In Munich he expanded the research area "Infection and Immunity" to a major research focus of his faculty.[ citation needed ] He co-initiated three Collaborative Research Programs and was from 1999-2006 speaker of the program "Target structures for selective Tumor-Interventions".[ citation needed ]
His honorary functions include: Presidency of the German Society of Immunology, Dean of the Faculty of Medicine (TUM), and Chairmen of the Science Advisory Board-IZKF-University Würzburg.[ citation needed ] A number of his pupills (n=13) are now heading university departments or other science-institutions; hence, Wagner and his pupills operate a creative academic school in Germany.[ citation needed ]
In 1988 Wagner received the Behring-Kitasato Prize from the Hoechst Japan,[ citation needed ] and in 2001 he was awarded an honorary doctorate by the University of Würzburg.[ citation needed ] In 2003 he received the "Order of Merit" of the Federal Republic of Germany.[ citation needed ] He has been an honorary member of the German Society of Immunology since 2007.[ citation needed ] He received the "Bavarian Order of Merit" in 2007.[ citation needed ] He is member of the Bavarian Academy of Sciences [3] [6] and the German Academy of Sciences Leopoldina.[ citation needed ] In 2009 he was Fellow of the A. Krupp Science Foundation in Greifswald/Baltic Sea,[ citation needed ] and in 2012 guest professor at the University of Marburg.[ citation needed ] Since 2011 he is TUM-Emeritus of Excellence.[ citation needed ] In 2013 he was awarded an honorary degree by the University of Bonn.[ citation needed ]
Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. They are single-pass membrane-spanning receptors usually expressed on sentinel cells such as macrophages and dendritic cells, that recognize structurally conserved molecules derived from microbes. Once these microbes have reached physical barriers such as the skin or intestinal tract mucosa, they are recognized by TLRs, which activate immune cell responses. The TLRs include TLR1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, TLR10, TLR11, TLR12, and TLR13. Humans lack genes for TLR11, TLR12 and TLR13 and mice lack a functional gene for TLR10. TLR1, TLR2, TLR4, TLR5, TLR6, and TLR10 are located on the cell membrane, whereas TLR3, TLR7, TLR8, and TLR9 are located in intracellular vesicles.
Pathogen-associated molecular patterns (PAMPs) are small molecular motifs conserved within a class of microbes, but not present in the host. They are recognized by toll-like receptors (TLRs) and other pattern recognition receptors (PRRs) in both plants and animals. This allows the innate immune system to recognize pathogens and thus, protect the host from infection.
Pattern recognition receptors (PRRs) play a crucial role in the proper function of the innate immune system. PRRs are germline-encoded host sensors, which detect molecules typical for the pathogens. They are proteins expressed, mainly, by cells of the innate immune system, such as dendritic cells, macrophages, monocytes, neutrophils and epithelial cells, to identify two classes of molecules: pathogen-associated molecular patterns (PAMPs), which are associated with microbial pathogens, and damage-associated molecular patterns (DAMPs), which are associated with components of host's cells that are released during cell damage or death. They are also called primitive pattern recognition receptors because they evolved before other parts of the immune system, particularly before adaptive immunity. PRRs also mediate the initiation of antigen-specific adaptive immune response and release of inflammatory cytokines.
The Bavarian Academy of Sciences and Humanities is an independent public institution, located in Munich. It appoints scholars whose research has contributed considerably to the increase of knowledge within their subject. The general goal of the academy is the promotion of interdisciplinary encounters and contacts and the cooperation of representatives of different subjects.
Myeloid differentiation primary response 88 (MYD88) is a protein that, in humans, is encoded by the MYD88 gene.
In immunology, an adjuvant is a substance that increases or modulates the immune response to a vaccine. The word "adjuvant" comes from the Latin word adiuvare, meaning to help or aid. "An immunologic adjuvant is defined as any substance that acts to accelerate, prolong, or enhance antigen-specific immune responses when used in combination with specific vaccine antigens."
Toll-like receptor 1 (TLR1) is a member of Toll-like receptors (TLRs), which is a family of pattern recognition receptors (PRRs) that form the cornerstone of the innate immune system. TLR1 recognizes bacterial lipoproteins and glycolipids in complex with TLR2. TLR1 is a cell surface receptor. TLR1 is in humans encoded by the TLR1 gene, which is located on chromosome 4.
Toll-like receptor 7, also known as TLR7, is a protein that in humans is encoded by the TLR7 gene. Orthologs are found in mammals and birds. It is a member of the toll-like receptor (TLR) family and detects single stranded RNA.
Lymphocyte antigen 96, also known as "Myeloid Differentiation factor 2 (MD-2)," is a protein that in humans is encoded by the LY96 gene.
Toll-like receptor 8 is a protein that in humans is encoded by the TLR8 gene. TLR8 has also been designated as CD288. It is a member of the toll-like receptor (TLR) family.
Toll-like receptor 9 is a protein that in humans is encoded by the TLR9 gene. TLR9 has also been designated as CD289. It is a member of the toll-like receptor (TLR) family. TLR9 is an important receptor expressed in immune system cells including dendritic cells, macrophages, natural killer cells, and other antigen presenting cells. TLR9 is expressed on endosomes internalized from the plasma membrane, binds DNA, and triggers signaling cascades that lead to a pro-inflammatory cytokine response. Cancer, infection, and tissue damage can all modulate TLR9 expression and activation. TLR9 is also an important factor in autoimmune diseases, and there is active research into synthetic TLR9 agonists and antagonists that help regulate autoimmune inflammation.
Shizuo Akira is a professor at the Department of Host Defense, Osaka University, Japan. He has made ground-breaking discoveries in the field of immunology, most significantly in the area of innate host defense mechanisms.
Stefan Hugo Ernst Kaufmann is a German immunologist and microbiologist and is one of the highly cited immunologists worldwide for the decade 1990 to 2000. He is amongst the 0.01% most cited scientists of ca. 7 million scientists in 22 major scientific fields globally.
Bernd Schröppel is a German former transplant nephrologist at the Mount Sinai Medical Center and the former medical director of the kidney pancreas transplant program at the Recanati/Miller Transplantation Institute at the Mount Sinai Medical Center in New York City. He is also a former assistant professor of nephrology at the Mount Sinai School of Medicine.
Gunther Hartmann is a German immunologist and clinical pharmacologist. Since 2007 he has been the Director of the Institute of Clinical Chemistry and Clinical Pharmacology at the University Hospital of the University of Bonn.
An interferon-stimulated gene (ISG) is a gene that can be expressed in response to stimulation by interferon. Interferons bind to receptors on the surface of a cell, initiating protein signaling pathways within the cell. This interaction leads to the expression of a subset of genes involved in the innate immune system response. ISGs are commonly expressed in response to viral infection, but also during bacterial infection and in the presence of parasites.It's currently estimated that 10% of the human genome is regulated by interferons (IFNs). Interferon stimulated genes can act as an initial response to pathogen invasion, slowing down viral replication and increasing expression of immune signaling complexes. There are three known types of interferon. With approximately 450 genes highly expressed in response to interferon type I. Type I interferon consists of INF-α, INF-β, INF-ω and is expressed in response to viral infection. ISGs induced by type I interferon are associated with viral replication suppression and increase expression of immune signaling proteins. Type II interferon consists only of INF-γ and is associated with controlling intracellular pathogens and tumor suppressor genes. Type III interferon consists of INF-λ and is associated with viral immune response and is key in anti-fungal neutrophil response.
An innate immune defect is a defect in the innate immune response that blunts the response to infection. These defects may occur in monocytes, neutrophils, natural killer cells, basophils, mast cells or complement proteins.
Regine Kahmann is a German microbiologist and was Director at the Max Planck Institute for Terrestrial Microbiology in Marburg from 2000 to 2019. She was made a Foreign Member of the Royal Society (ForMRS) in 2020.
Tim Dominik Sparwasser is a German physician, microbiologist and infection immunologist. In 2018, he became director of the Institute for Medical Microbiology and Hygiene (IMMH) in Mainz.
Roman Dziarski is a Polish-born American immunologist and microbiologist. He is best known for his research on innate immunity and bacterial peptidoglycan, for discovering the family of human peptidoglycan recognition proteins, which comprises PGLYRP1, PGLYRP2, PGLYRP3, and PGLYRP4, and for defining the functions of these proteins.