Ciba Foundation Symposium 118 - Biochemistry of Macrophages by CIBA Foundation Symposium, Symposium

By CIBA Foundation Symposium, Symposium

Chapter 1 the 1st Line of Defence: Chairman's creation (pages 1–6): Zanvil A. Cohn
Chapter 2 Specificity of motion of Colony?Stimulating components within the Differentiation of Granulocytes and Macrophages (pages 7–28): Nicos A. Nicola and Donald Metcalf
Chapter three motion of the Colony?Stimulating issue, CSF?1 (pages 29–41): E. Richard Stanley
Chapter four Actin Filament structure and routine in Macrophage Cytoplasm (pages 42–53): John H. Hartwig
Chapter five Localization and serve as of Tissue Macrophages (pages 54–67): Siamon Gordon, Paul R. Crocker, Lynn Morris, Szu Hee Lee, V. Hugh Perry and David A. Hume
Chapter 6 Macrophage Antigens and the influence of a Macrophage Activating issue, Interferon?? (pages 68–88): Nancy Hogg, Yogi Selvendkan, Graeme Dougherty and Catherine Allen
Chapter 7 Heterogeneity of Human and Murine Fc?, Receptors (pages 89–101): Jay C. Unkeles
Chapter eight the significance of the Mac?1, LFA?1 Glycoprotein family members in Monocyte and Granulocyte Adherence, Chemotaxis, and Migration into Inflammatory websites: Insights from an scan of Nature (pages 102–126): Timothy A. Springeii and Donald C. Anderson
Chapter nine interplay and law of Macrophage Receptors (pages 127–140): R. A. B. Ezekowitz and S. Gordon
Chapter 10 rules of supplement Protein Biosynthesis in Mononuclear Phagocytes (pages 141–154): Harvey R. Colten, Robert C. Perlmutter, David H. Schlessinger and F. classes Cole
Chapter eleven The phone and Molecular Biology of Apolipoprotein E Synthesis via Macro Phages (pages 155–171): Zena Werb, Jennie R. Chin, Relko Takemura, Rosa Laura Oropeza, Dorothy F. Bainton, Paula Stenberg, John M. Taylor and Catherine Reardon
Chapter 12 breathing reaction of Phagocytes: Terminal NADPH Oxidase and the Mechanisms of its Activation (pages 172–195): Flllppo Kossi, Paolo Bellavite and Emanuele Papini
Chapter thirteen Bacterial Lipopolysaccharides regulate sign Transduction within the Arachidonic Acid Cascade in Macrophages (pages 196–210): Alan A. Aderem and Zanvil. A. Coiin
Chapter 14 Secretion of poisonous Oxygen items by means of Macrophages: Regulatory Cytokines and their results at the Oxidase (pages 211–241): Carl F. Nathan and Shohko Tsunawaki
Chapter 15 Chairman's last comments (pages 242–243): Zanvil A. Cohn

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In addition, considerable sequence homology exists between the amino terminal amino acid sequences of murine and human CSF-1 ( J . E. Stricklcr et al. unpublished work 1985). m. per ng) without loss of biological or antibody-binding activity (reviewed in Stanley & Cuilbert 1981). 35. T h e binding is of high affinity ( K dd M) and is not competed for by other known CSF subclasses. growth ACTION OF CSF-I 31 factors or hormones. It is saturable within 1 h at a CSF-1 concentration of 2nM (Guilbert & Stanley 1980).

One message appears to produce a classic secreted protein product, GM-CSF and Multi-CSF. In both cases there is an alternative cDNA which appears to have some of the hallmarks of an integral membrane protein. It certainly has the GM-CSF and Multi-CSF sequence but at its N-terminal end i t codes for a hydrophobic region preceded by a sequence containing several charged groups. This is characteristic of a membrane-bound protein. That would be very interesting if, as you suggest, forms of GM-CSF and Multi-CSF produced in the bone marrow are membrane-bound and their effects are localized by cell-cell contact, whereas under other circumstances you can produce a secreted form of CSF which circulates and activates granulocytes and macrophages in the periphery.

G. down-regulation). It reflects a developmentally associated increase in the capacity of cells to express the receptor that is correlated with acquisition of responsiveness to CSF-1 alone. As the occurrence of the CSF-1 receptor on later haemopoietic cells is restricted to the mononuclear phagocytic lineage, its increased expression represents a very early marker of determination t o this lineage. + + Acknowledgements This work was supported by grants CA26504 and CA325SI from the National Cancer Institute and the AECOM Cancer Centre Core Grant.

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