Protein and cell engineering of components of the human immunoglobulin E receptor/effector system: applications for therapy and diagnosis.

Adaptive immune responses characterised by the synthesis of antibodies of the immunoglobulin E (IgE) isotype play an important role in type I hypersensitivity disorders and parasitic infestations, diseases which have an significant socioeconomic impact world-wide. This paper considers potential applications of recent advances in our understanding of the origin of isotype specific immune responses which emerged as a result of cell and protein engineering studies on components of the human IgE/receptor/effector system. Furthermore, the identification of the receptor binding regions in IgE as a result of the development of a stable assay system has important applications for the design of rational therapeutic interventions in allergy and asthma, the treatment of mast cell tumours, and the establishment of procedures for the selective isolation of cells expressing the high-affinity receptor for IgE for functional studies.

[1]  A. Saxon,et al.  Combined diesel exhaust particulate and ragweed allergen challenge markedly enhances human in vivo nasal ragweed-specific IgE and skews cytokine production to a T helper cell 2-type pattern. , 1997, Journal of immunology.

[2]  M. Moffatt,et al.  Asthma--An Epidemic in the Absence of Infection? , 1997, Science.

[3]  B. Helm,et al.  Potential allergens stimulate the release of mediators of the allergic response from cells of mast cell lineage in the absence of sensitization with antigen‐specific IgE , 1996, European journal of immunology.

[4]  A. Saxon,et al.  Enhanced nasal cytokine production in human beings after in vivo challenge with diesel exhaust particles. , 1996, The Journal of allergy and clinical immunology.

[5]  E. Padlan,et al.  Identification of the High Affinity Receptor Binding Region in Human Immunoglobulin E (*) , 1996, The Journal of Biological Chemistry.

[6]  A. Saxon,et al.  Diesel exhaust particles induce local IgE production in vivo and alter the pattern of IgE messenger RNA isoforms. , 1994, The Journal of clinical investigation.

[7]  P. Monk,et al.  Defective protein phosphorylation and Ca2+ mobilization in a low secreting variant of the rat basophilic leukemia cell line. , 1994, The Journal of biological chemistry.

[8]  J. Haddow,et al.  Association between exposure to environmental tobacco smoke and exacerbations of asthma in children. , 1993, The New England journal of medicine.

[9]  B. Helm,et al.  Human IgE mediates stimulus secretion coupling in rat basophilic leukemia cells transfected with the α chain of the human high‐affinity receptor , 1993 .

[10]  P. Holt,et al.  The distribution of IgE plasma cells in lymphoid and non-lymphoid tissues of high-IgE responder rats: differential localization of antigen-specific and 'bystander' components of the IgE response to inhaled antigen. , 1992, Immunology.

[11]  E. Padlan,et al.  The nature and importance of the inter‐ε chain disulfide bonds in human IgE , 1991, European journal of immunology.

[12]  O. Zetterström,et al.  Another smoking hazard: raised serum IgE concentration and increased risk of occupational allergy. , 1981, British medical journal.

[13]  E. Chi,et al.  Eosinophil peroxidase-induced mast cell secretion , 1980, The Journal of experimental medicine.

[14]  A. Saxon,et al.  Enhanced human IgE production results from exposure to the aromatic hydrocarbons from diesel exhaust: direct effects on B-cell IgE production. , 1995, The Journal of allergy and clinical immunology.