Conclusions

Defective or exaggerated activation of M0 contributes to pathogenesis of a wide range of immunological and other diseases. Key molecules involved in this process provide suitable targets for therapy. Many questions regarding the selective expression of M0 genes and their regulation by extrinsic and intrinsic cellular processes remain for further study. The concepts outlined above should serve as a guide for further dissection of this complex process, and its relation to other aspects of Mb function.

See also: Adhesion molecules; Adjuvants; Antigen, entry into the body; Antigen-presenting cells; Antigens, cell surface; BCG; Biozzi mice; Complement, alternative pathway; Cell-mediated immunity; Chemokines; Cytokine assays; Cytokine genes, regulation of; Cytokine receptors, soluble; Cytokines; Cytokine receptors; Cytotoxicity, mechanisms of; Dendritic cells; Endotoxin (lipopolysaccharide (LPS)); Fas (CD95) and fas ligand; Fc receptors; Glucocorticoids; Granulocyte-macrophage colony stimulating factor (GM-CSF); Granuloma; Immunopathol-ogy; Inflammatory bowel disease; Interferon <*; Interferon P; Interferon 7; Interleukin 1 and its receptors; interleukin 4; Interleukin 10 and its receptor; Lifespan of immune cells and molecules; Listeria, infection and immunity; Macrophage colony stimulating factor (CSF-1); Microbicidal mechanisms, oxygen-dependent; Microbicidal mechanisms, oxygen-independent; Microenvironment; Monocyte chemot-actic protein 1 (MCP-1); Monocytes; Mononuclear phagocyte system; Mycobacteria, infection and immunity; Myeloid antigens; Neutrophils; Nitric oxide; Phagocytosis; Sarcoidosis; Septic shock; Spleen; Stromal cells; Targeting of immunological agents; Tolerance, peripheral; Tumor necrosis factor a; TNF receptors; Viruses, immunity to; Chemotaxis of macrophages and monocytes.

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