Allergy , Edition: 4th ed. by S. Holgate, et. al.

By S. Holgate, et. al.

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Additional info for Allergy , Edition: 4th ed.

Sample text

Apoptosis, or programmed cell death, is a mechanism for resolution of allergic or other forms of inflammation. Apoptotic cells are removed by neighboring phagocytic cells without loss of their potentially harmful cell contents. In contrast to apoptosis, necrosis is a pathological form of cell death resulting from acute cellular injury. Necrosis is always associated with loss of intracellular mediators and enzymes into the extracellular environment and the consequential potential induction of an inflammatory response.

22; 3rd edition) to elements of the contents of this chapter covered in the 3rd edition. The chapter has been substantially revised for this 4th edition. Further reading Bochner BS, Gleich GJ. What targeting eosinophils has taught us about their role in diseases. J Allergy Clin Immunol 2010; 126:16–25. Finkelman FD, Hogan SP, Hershey GKK, et al. Importance of cytokines in murine allergic airway disease and human asthma. J Immunol 2010; 184:1663–1674. Geissmann F, Manz MG, Jung S, et al. Development of monocytes, macrophages, and dendritic cells.

The heritability of many allergic disease related phenotypes has also been studied and has shown that genetic factors influence not just disease susceptibility per se but all aspects of disease. For example, for asthma, heritability studies have shown there is genetic influence in many aspects, from susceptibility to atopy and regulation of total and specific IgE levels, to blood eosinophil levels, susceptibility to asthma per se, degree of bronchial hyperresponsiveness, severity of asthma symptoms, and even risk of mortality from asthma.

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