Grooten Lab - Molecular Immunology

Research field: Protagonist and antagonist functions of activated macrophages in immune inflammatory disorders

Group leader: Prof. Dr. Johan Grooten

Tel:+32 9 33 13 689 - Fax:+32 9 221 76 73
E-mail: Johan.Grooten.spam.detractor@UGentspam.corruptor.be

(Note: Johan Grooten's lab is part of the UGent Department of Biomedical Molecular Biology but not a VIB unit)

Research topic

Due to their phagocytic activity, macrophages (MΦ) are an important component of the innate immune defense. Toll-like receptors and other pattern recognition receptors allow the cells to discriminate non-self from modified-self, resulting in engulfment and clearance of infectious agents. Signal transduction driving gene expression confers to the activated MΦ additional inflammatory effector functions. Responsiveness to T lymphocyte-derived cytokines and other adaptive immune effectors, such as antibody-antigen complexes, further diversifies the resultant MΦ activation. When appropriately activated, presentation of engulfed antigens to Th-lymphocytes may raise tolerogenic responses or modify the nature of the immune inflammatory response.
In view of this multiplicity of MΦ functions and responsiveness, our research group explores the bi-directional relationship between Mf activation by local inflammatory conditions, and steering by the activated MΦ of the inflammatory response and underlying immune reactivity. Gene expression profiling of MΦ isolated from inflamed airways (models of asthma, pneumonia, COPD) with MΦ focus arrays made in-house is combined with functional analysis by macrophage transfer experiments and local application of MΦ-targeted triggers. Special emphasis is placed on the regulatory role of MΦ at the innate-adaptive immune interphase, thus interfering with the upstream causal immune reactivity as well as with the downstream inflammatory process.

Area of expertise

  • Asthma and bronchial inflammation mouse models
  • Transcriptome profiling by cDNA arrays
  • Macrophage and T lymphocyte functions
  • IL-15, eicosanoids and other mediators
  • Macrophage Fc-gamma receptors

Technology transfer potential

  • Therapeutic targets for treatment of asthma
  • Molecular targets for inflammation diagnosis/theragnosis
  • Molecular targets for drug screening, adjuvant development, and others


Selected publications

  1. Sehra et al., Airway IgG counteracts specific and bystander allergen-triggered pulmonary inflammation by a mechanism dependent on FcgR and IFN-gamma. J Immunol, 171, 2080-2089, 2003.
  2. Pynaert et al., Antigen presentation by local macrophages promotes nonallergic airway responses in sensitized mice. Am J Respir Cell Mol Biol 29, 634-641, 2003.
  3. Dooms et al., Interleukin-15 redirects the outcome of a tolerizing T cell stimulus from apoptosis to anergy. Blood 96, 1006-1012, 2000.
  4. Peppelenbosch et al., Macrophages present pinocytosed exogenous antigen via MHC class I whereas antigen ingested by receptor-mediated endocytosis is presented via MHC class II. J Immunol 165, 1984-1991, 2000.
  5. Desmedt et al., Macrophages induce cellular immunity by activating Th1 cell responses and suppressing Th2 cell responses. J Immunol 160, 5300-5308, 1998.