Macrophages in Anti-inflammation : molecular mechanisms, apoptosis, and tolerance induction : 2nd Teupitzer Colloquium September 2-4, 1999
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Bibliographic Information
Macrophages in Anti-inflammation : molecular mechanisms, apoptosis, and tolerance induction : 2nd Teupitzer Colloquium September 2-4, 1999
（Pathobiology : jounral of immunopathology, molecular and cellular biology, vol. 67,
S. Karger, 2000
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Description and Table of Contents
Description
During the last two decades, anti-infammatory mechanisms have moved from a neglected field of immunology to the forefront of inflammation research. Anti-inflammatory mechanisms function in various ways: they protect against unwanted immune reactions and contain inflammatory reactions once these are induced. Finally, they secure downregulation and healing after the succesful elimination of a noxious agent. Specialized, alternatively activated macrophages play a major role in these processes. Alternatively activated macrophages tend toward preferential secretion of anti-inflammatory cytokines; are capable of removing apoptotic cells and tissue debris without inflammation; and can - along with deactivated immature dendritic cells - deliver tolerance signals to T-cells. Thus, anti-inflammatory macrophages are attractive candidates for a cell-based vaccination therapy of allergic and autoimmune diseases. Further, the molecular repertoire of alternatively activated antigen-presenting cells may be used to develop new drugs for inflammatory disease therapy. The present volume brings together the latest findings of researchers and clinicians world-wide in the area of anti-inflammatory macrophage and dendritic cell biology. Mechanisms of antigen-presenting cell-dependent anti-inflamatory reactions, in conjunction with immunotolerance and healing are discussed. The aim is to present the newest and most relevant developments in deciphering and making therapeutic use of these mechanisms. The book introduces the emerging concept of an alternative activation pathway of antigen-presenting cells that parallels the Th1/Th2 dichotomy.
Table of Contents
- Alternative versus classical activation of macrophages, S. Goerdt et al
- fighting infection - the role of lipopolysaccharide binding proteins CD14 and LBP, C. Schutt
- the regulatory role of MRP8 ( S100A8) and MRP14 (S100A9) in the transendothelial migration of human leukocytes, C. Kerkhoff et al
- the contact of human macrophages with extracellular matrix proteins selectively induces expression of proinflammatory cytokines, R. Schiffer et al
- ATP-binding cassette transporter A1 (ABCA1) in macrophages - a dual function in inflammation and lipid metabolism? G. Schmitz et al
- regulation of macrophage gene expression by pro- and anti-inflammatory cytokines, T.A. Hamilton et al
- alternative activation of macrophage by IL-10, R. Stumpo et al
- phenotypic analysis of IL-10 treated macrophages using the monoclonal antibodies RFD1 and RFD7, L.S. Taams et al
- comparison of monocyte functions after LPS- or IL-10 induced reorientation -importance in clinical immunoparalysis, K. Wolk et al
- the scavenger receptor CD163 - regulation, promoter structure and gnomic organisation, M. Ritter et al
- glucocorticoid receptor ligand binding in monocytic cells using a microplate assay, J. Jansen et al
- suppressive antigen-presenting cells in Helminth infection, A.S. MacDonald et al
- the regulatory role of the antigen-presenting cell in the development of hepatic immunopathology during infection with schistosoma mansoni, M.J. Stadecker
- experimental African trypanosomiasis - differences in cytokine and nitric oxide production by macrophages from resistant and susceptible mice, H. Tabel et al
- balanced macrophage activation hypothesis - a biological model for development of drugs targeted at macrophage functional states, M.S. McGarth, V. Kodelja
- stimulatory and inhibitory maturation of human macrophage-derived dendritic cells, A. Chakraborty et al
- M-DC8+ leukocytes - a novel human dendritic cell population, K. Schakel et al
- the role of cytokines in monocyte apoptosis, H.-D. Fald et al. (Part contents).
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