The Biology and Pathology of Innate Immunity Mechanisms

In recent years increased scientific attention has been given to immediate defense mechanisms based on non-clonal recognition of microbial components. These mechanisms constitute the innate immunity arm of the body s defense. Identification of pathogens by these mechanisms involves primarily receptors recognizing sugar moieties of various microorganisms. Innate immunity based mechanisms are essential for the existence of multicellular organisms. They are evolutionarily conserved and designed to provide immediate protection against microbial pathogens to eradicate infection. Activation of innate immunity is crucial for transition to specific immunity and for its orientation, and to assist the specific immune response in the recognition of pathogens and their destruction. Innate immunity is regularly involved in the arrest of bacterial, mycotic, viral and parasitic infections, giving the specific immune response time to become effective. It becomes critically essential in immunocompromised patients who fail to mount specific immune responses due to congenital or acquired immunodeficiencies as a result of chemotherapy, dialysis, immunosuppressive drugs, or HIV infection. The Innate Immunity arsenal constitutes polymorphonuclear and mononuclear phagocytes, mast cells, the complement system, Natural Killer cells, antimicrobial peptides, and presumably a subset of T lymphocytes with TCRl receptors.

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Preface. I: Pattern Recognition, Receptors and Collectins in Innate Immunity. 1. Mannose receptor and scavenger receptor: two macrophage pattern recognition receptors with diverse functions in tissue homeostasis and host defense; S.A. Linehan, et al. 2. Complement receptor 3 (CR3): a public transducer of innate immunity signals in macrophages; E. Yefenof. 3. The role of C-type lectins in the innate immunity against pulmonary pathogens; I. Ofek, et al. 4. Modulation of nitric oxide production by lung surfactant in alveolar macrophages; M. Kalina, et al. 5. Development of chimeric collectins with enhanced activity against influenza A virus; K. Hartshorn, et al. 6. Initial steps in Streptococcus pneumoniae interaction with and pathogenicity to the host; M. Shani-Sekler, et al. II: Host Cells and Cytokines in Innate Immunity. 7. Role of cytokines in the maturation and function of macrophages: effect of GM-CSF and IL-4; Y. Keisari, et al. 8. Mast cell modulation of the innate immune response to enterobacterial infection; S.N. Abraham, R. Malaviya. 9. The NADPH oxidase diaphorase activity in permeabilized human neutrophils and granulocytic like PLB-985 cells; I. Pessach, R. Levy. 10. Activation of cytosolic phospholipase A2 by opsonized zymosan in human neutrophils requires both ERK and p38 MAP-kinase; I. Hazan-Halevy, R. Levy. 11. Cytosolic phospholipase A2 is required for the activation of the NADPH oxidase associated H+ channel in phagocyte-like cells; R. Levy, et al. 12. The role of NK cells in innate immunity; N. Lieberman, O. Mandelboim. 13. Similarities and dissimilarities between humans and mice looking at adhesion molecules efects; A. Etzioni, et al. 14. The role of dendritic cells at the early stages of Leishmania infection; H. Moll. 15. DNA-based vaccines: role of dendritic cells in antigen presentation; L. Paul, A. Porgador. 16. Distinct patterns of IL-1&agr; and IL-1&bgr; organ distribution &endash; a possible basis for organ mechanisms of innate immunity; M. Hacham, et al. III: Antimicrobial Peptides. 17. Structure and biology of cathelicidins; M. Zanetti, et al. 18. Structure activity relationship study of polymyxin B nonapeptide; H. Tsubery, et al. IV: Innate Immunity in the Compromised Host. 19. The clinical significance of neutrophil dysfunction; B. Wolach, et al. 20. Clinical significance of function aberrations in macrophages and NK cells, in type-1 cytokines and in lectin-binding molecules; Z. Handzel. 21. Klebsiella infections in the immunocompromised host; H. Sahly, et al. V: Innate Immunity Components in Cancer. 22. Macrophage &endash; recognized molecules of apoptotic cells are expressed at higher level in AKR lymphoma of aged as compared to young mice; O. Itzhaki, et al. 23. Sensitivity to macrophages decreases with tumor progression in the AKR lymphoma; T. Kaptzan, et al. 24. Opposing effects of IL-1&agr; and IL-1&bgr; on malignancy patterns; tumor cell-associated IL-1&agr; potentiates anti-tumor immune responses and tumor regression, whereas IL-1&bgr; potentiates invasiveness; R.N. Apte, et al.<