Michael Stassen

ORCID: 0000-0001-6610-6439
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About
Contact & Profiles
Research Areas
  • Mast cells and histamine
  • Asthma and respiratory diseases
  • Immune Cell Function and Interaction
  • Allergic Rhinitis and Sensitization
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Food Allergy and Anaphylaxis Research
  • IL-33, ST2, and ILC Pathways
  • Immune Response and Inflammation
  • Antifungal resistance and susceptibility
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Pediatric health and respiratory diseases
  • Inhalation and Respiratory Drug Delivery
  • NF-κB Signaling Pathways
  • Inflammation biomarkers and pathways
  • Cytokine Signaling Pathways and Interactions
  • Protein Tyrosine Phosphatases
  • Antimicrobial Peptides and Activities
  • Eosinophilic Esophagitis
  • Signaling Pathways in Disease
  • Respiratory viral infections research
  • Immune cells in cancer
  • Peptidase Inhibition and Analysis
  • Neonatal Respiratory Health Research
  • Cytomegalovirus and herpesvirus research

University Medical Center of the Johannes Gutenberg University Mainz
2014-2023

Johannes Gutenberg University Mainz
2014-2023

University Medical Center
2015

Institute of Immunology
2004-2015

Darmstadt University of Applied Sciences
1996

Princeton University
1993

Cavendish University Uganda
1993

Syracuse University
1993

Purdue University West Lafayette
1993

McMaster University
1993

A subpopulation of peripheral human CD4+CD25+ T cells that expresses CD45RO, histocompatibility leukocyte antigen DR, and intracellular cytotoxic lymphocyte–associated (CTLA) 4 does not expand after stimulation markedly suppresses the expansion conventional in a contact-dependent manner. After activation, express CTLA-4 on surface detectable for several weeks. These show G1/G0 cell cycle arrest no production interleukin (IL)-2, IL-4, or interferon (IFN)-γ either protein mRNA levels. The...

10.1084/jem.193.11.1285 article EN The Journal of Experimental Medicine 2001-06-04

Naturally occurring regulatory T cells (T reg cells) are a thymus-derived subset of cells, which crucial for the maintenance peripheral tolerance by controlling potentially autoreactive cells. However, underlying molecular mechanisms this strictly cell contact–dependent process still elusive. Here we show that naturally harbor high levels cyclic adenosine monophosphate (cAMP). This second messenger is known to be potent inhibitor proliferation and interleukin 2 synthesis in Upon coactivation...

10.1084/jem.20062129 article EN The Journal of Experimental Medicine 2007-05-14

Regulatory CD4+CD25+ T cells (Treg) are mandatory for maintaining immunologic self-tolerance. We demonstrate that the cell-cell contact–mediated suppression of conventional CD4+ by human CD25+ Treg is fixation resistant, independent from membrane-bound TGF-β but requires activation and protein synthesis cells. Coactivation with cell–depleted results in anergized turn inhibit conventional, freshly isolated helper (Th) This infectious suppressive activity, transferred via cell contact,...

10.1084/jem.20020394 article EN The Journal of Experimental Medicine 2002-07-15

Down-regulation of autoreactive T cell responses in vivo includes cell-contact-dependent as well contact-independent mechanisms. Infectious tolerance is a contact-dependent mechanism used by naturally occurring CD25(+) regulatory cells (Tregs) to confer suppressive activity upon conventional CD4(+) thereby generating secondary helper suppressor cells(Th(sup)), which inhibit activation via soluble mediators. Here, we describe two distinct subsets human Tregs, characterized expression either...

10.1002/eji.200324656 article EN European Journal of Immunology 2004-04-05

Abstract Mast cells, due to their ability produce a large panel of mediators and cytokines, participate in variety processes adaptive innate immunity. Herein we report that primary murine bone marrow-derived mast cells activated with ionomycin or IgE-Ag the bacterial endotoxin LPS strongly enhances expression IL-9 IL-13, but not IL-4. This costimulatory effect is absent derived from LPS-hyporesponsive mouse strain BALB/c-LPSd, although these proinflammatory cytokine IL-1 can still substitute...

10.4049/jimmunol.166.7.4391 article EN The Journal of Immunology 2001-04-01

Mast cells can play detrimental roles in the pathophysiology and mortality observed anaphylaxis other Th2-dominated allergic diseases. In contrast, these contribute to protective host defense mechanisms against parasitic worm infections. After IgE/Ag activation, mast produce multiple cytokines that may enhance inflammations, while a similar panel of Th2-related support immunological strategies parasites. Here we report primary mouse bone marrow-derived activated by ionomycin or IgE/Ag,...

10.4049/jimmunol.164.11.5556 article EN The Journal of Immunology 2000-06-01

The phenotype of NFATc2−/− c3−/− (double knockout [DKO]) mice implies a disturbed regulation T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. population CD4+ CD25+ cells from DKO lacks regulatory capacity, except small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family–related gene (GITR) CD25. However, neither wild-type nor (T reg cells) are able to suppress proliferation CD25− helper cells....

10.1084/jem.20041538 article EN The Journal of Experimental Medicine 2005-01-17

Naturally occurring regulatory T cells (nTreg cells) are crucial for the maintenance of peripheral tolerance. We have previously shown that a key mechanism their suppressive action is based on contact-dependent transfer cAMP from nTreg to responder cells. Herein, we further elucidate important role properties Prevention degradation by application phosphodiesterase 4 inhibitor rolipram led strongly increased potency Th2 in vitro and vivo. Detailed analyses revealed caused, presence cells,...

10.4049/jimmunol.0803310 article EN The Journal of Immunology 2009-03-19

The lungs are a noted predilection site of acute, latent, and reactivated cytomegalovirus (CMV) infections. Interstitial pneumonia is the most dreaded manifestation CMV disease in immunocompromised host, whereas immunocompetent host lung-infiltrating CD8 T cells confine infection nodular inflammatory foci prevent viral pathology. By using murine as model, we provide evidence for critical role mast (MC) recruitment protective to lungs. Systemic triggered degranulation selectively infected MC....

10.1371/journal.ppat.1004100 article EN cc-by PLoS Pathogens 2014-04-24

Abstract Recently, the Th2-type cytokine IL-9 was identified by genetic mapping analyses as a key mediator that determines susceptibility to asthma. This has been further supported data from IL-9-transgenic mice in which overexpression of lung causes airway inflammation, mast cell hyperplasia, and bronchial hyperresponsiveness. In an accompanying paper, we demonstrate murine bone marrow-derived cells (BMMC) after stimulation with either ionomycin, combination ionomycin IL-1, or via IgE-Ag...

10.4049/jimmunol.164.11.5549 article EN The Journal of Immunology 2000-06-01

Abstract CD25+ T regulatory (Treg) cells play a central role regarding the maintenance of peripheral tolerance via suppression autoaggressive CD4+ cells, CD8+ and Th1 cells. In this study we demonstrate that Treg can also suppress differentiation murine conventional toward Th2 in contact-dependent manner. However, cytokine production proliferation established could not be inhibited by freshly isolated whereas strong inhibition differentiated vitro preactivated observed. Inhibition both is...

10.4049/jimmunol.173.1.267 article EN The Journal of Immunology 2004-07-01

By virtue of their ability to express a plethora biologically highly active mediators, mast cells (MC) are involved in both adaptive and innate immune responses. MC-derived Th2-type cytokines thought act as local amplifiers Th2 reactions, including chronic inflammatory disorders such allergic asthma, whereas TNF-alpha is critical initiator antimicrobial defense. In this study, we demonstrate that the transcription factors NFATc1 NFATc2 part MC-specific signaling network regulates expression...

10.4049/jimmunol.177.10.6667 article EN The Journal of Immunology 2006-11-15

Ticks developed a multitude of different immune evasion strategies to obtain blood meal. Sialostatin L is an immunosuppressive cysteine protease inhibitor present in the saliva hard tick Ixodes scapularis. In this study, we demonstrate that sialostatin strongly inhibits production IL-9 by Th9 cells. Because could show recently Th9-derived essentially involved induction asthma symptoms, was used for treatment experimental asthma. Application model almost completely abrogated airway...

10.4049/jimmunol.1100529 article EN The Journal of Immunology 2012-02-11

IL-4 and IL-13 play a crucial role during allergic asthma. Both cytokines can be produced by T cells variety of cell types the innate immune system. The relative contribution T-cell-derived vs IL-4/IL-13 for inflammation airway hyperreactivity remains unclear. We compared severity OVA/alum-induced lung in WT BALB/c mice to that lack expression only (4-13Tko) or all (4-13ko). was required IgG1 IgE production, recruitment eosinophils basophils lung, goblet hyperplasia, Muc5ac, Clca3, RELMβ,...

10.1111/all.12705 article EN Allergy 2015-07-27

Dual specificity phosphatase DUSP1 (otherwise known as mitogen-activated 1 or MKP-1) dephosphorylates MAPKs, particularly p38, and negatively regulates innate immunity. Recent studies have shown that the gene is transcriptionally up-regulated by glucocorticoids (GCs) antiinflammatory action of GCs impaired in DUSP1-/- mice. Here we show GC-mediated dephosphorylation ERK-1 ERK-2 activated IgE receptor cross-linking unimpaired bone marrow-derived mast cells (BMMCs) Dephosphorylation...

10.1210/me.2007-0067 article EN Molecular Endocrinology 2007-07-17

Mast cells are thought to contribute allergic airway disease. However, the role of mast cell-produced mediators, such as tumour necrosis factor (TNF), for development disease is unclear. In order define in acute two strains cell-deficient mice (Kit W/Wv and Kit W-sh/W-sh ) were studied. Compared with their wild-type littermates, developed significantly lower responsiveness methacholine less inflammation goblet cell metaplasia, following sensitisation absence adjuvant challenge. Transfer bone...

10.1183/09031936.00058907 article EN European Respiratory Journal 2007-12-19
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