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Chapter 5 : Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment

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Abstract:

Allergic inflammation, caused by development of an allergen-induced immune response, is largely driven via immunoglobulin E (IgE)-dependent mechanisms. It manifests clinically as asthma, rhinoconjunctivitis (more commonly known as hay fever), allergic skin inflammation (the main example of which is atopic dermatitis), food allergy, urticaria, and/or anaphylaxis, with several known disease variants caused by different underlying cellular and molecular mechanisms ( ). Increased levels of circulating IgE, allergen-specific IgE reactivity profiles measured with radioallergosorbent tests and positive skin prick tests for specific allergens, together with auxiliary ex vivo and in vitro mast cell and basophil activation functional readouts, support the importance of IgE antibodies in the clinical manifestation of allergies ( ). Allergic inflammation can be local (that is, within the target organ), as is the case for allergic rhinoconjunctivitis and allergic asthma, or systemic, as is the case for anaphylaxis. The etiology of allergic immune responses has been shown to be influenced by several factors, including genetic susceptibility ( ), route of exposure, dose of the allergen, and in some cases, structural characteristics of the allergen ( ).

Citation: Karagiannis S, Karagiannis P, Josephs D, Saul L, Gilbert A, Upton N, Gould H. 2015. Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment, p 75-102. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0006-2012
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Figure 1

Omalizumab blocks IgE-mediated mast cell activation. The allergic response mediated by multivalent allergen-IgE-FcεRI complex formation on the surface of mast cells triggers cross-linking of FcεRI, leading to downstream signaling events potentiated by the β and γ chains (left). These entail phosphorylation (P) by Src kinases and cellular activation through RhoGTPases and mitogen-activated protein kinase pathways, leading to mast cell degranulation and the rapid release of a range of vasoactive amines (e.g., histamine), prostaglandins, leukotrienes, cytokines, and chemokines, inducing and maintaining allergic inflammatory responses. Omalizumab, a humanized IgG1 monoclonal antibody that recognizes an epitope in the Cε3 region of IgE, can block the binding of circulating IgE to FcεRI, sequestering free and allergen-bound IgE (right). These interactions prevent allergen-IgE-FcεRI complex formation on the surface of mast cells and interfere with the signaling cascades that trigger degranulation and the onset of IgE-mediated allergic inflammatory cascades. Syk, spleen tyrosine kinase; AKT, Ak strain thymoma serine/threonine-specific protein kinase; ERK, extracellular signal-regulated kinase; JNK, Jun N-terminal protein kinase; P, phosphorylation.

Citation: Karagiannis S, Karagiannis P, Josephs D, Saul L, Gilbert A, Upton N, Gould H. 2015. Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment, p 75-102. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0006-2012
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Figure 2

IgG4 antibodies induced by allergen immunotherapies modulate IgE-mediated activation of effector cells. The allergic response mediated by multivalent allergen-IgE FcεRI complex assembly and downstream signaling events leading to release of inflammatory mediators (left) may be blocked by adaptive immune responses triggered in response to SIT with recombinant antigens. IgG4 antibodies, induced following SIT, could compete with IgE for binding to allergens and prevent the formation of allergen-IgE-FcεRI complexes on the surface of effector cells, blocking effector functions such as degranulation (right). Syk, spleen tyrosine kinase; AKT, Ak strain thymoma serine/threonine-specific protein kinase; ERK, extracellular signal-regulated kinase; JNK, Jun N-terminal protein kinase; P, phosphorylation.

Citation: Karagiannis S, Karagiannis P, Josephs D, Saul L, Gilbert A, Upton N, Gould H. 2015. Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment, p 75-102. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0006-2012
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Tables

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TABLE 1

Interactions of omalizumab with IgE, the resulting mechanisms of action, and clinical effects of treatment in patients with allergies

Citation: Karagiannis S, Karagiannis P, Josephs D, Saul L, Gilbert A, Upton N, Gould H. 2015. Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment, p 75-102. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0006-2012
Generic image for table
TABLE 2

Active phase II, III, and IV interventional clinical studies for antibody immunotherapies of allergic diseases in 2012

Citation: Karagiannis S, Karagiannis P, Josephs D, Saul L, Gilbert A, Upton N, Gould H. 2015. Immunoglobulin E and Allergy: Antibodies in Immune Inflammation and Treatment, p 75-102. In Crowe J, Boraschi D, Rappuoli R (ed), Antibodies for Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.AID-0006-2012

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