Immunoglobulin E: Biosynthesis and Immunological Mechanisms of IgE-Mediated Hypersensitivity

Ishizaka, Kimishige

doi:10.1007/978-1-4684-0988-8_5

Cited by 10 publications

(4 citation statements)

References 64 publications

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“…On one end of the scale are immediate hypersensitivity reactions, which have been shown to be due to the rapid release of vasoactive amines and other mediators from degranulated mast cells that have been passively sensitized with specific antibody of the IgE isotype (1)(2)(3). On the other end of the spectrum are cell-mediated hypersensitivity reactions, in which antigen-specific immune Lyl T cells recruit other inflammatory cells to the site ofthe antigen (4).…”

mentioning

confidence: 99%

Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

Ptak¹,

Askenase²,

Rosenstein³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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The fact that T cell-dependent activation of mast cells occurs in delayed-type hypersensitivity led us to investigate whether a T cell product could mimic some ofthe functions ofIgE. We report that 24-or 48-hr cultures of T cells from mice immunized optimally for delayed-type hypersensitivity resulted in release of an antigen-binding factor that transferred the ability to elicit an antigen-specific immediate hypersensitivity-like skin reaction in normal recipients. The responsible factor was concentrated and purified by affinity chromatography on antigen columns and was distinguished from immunoglobulin by several criteria: (i) it was released by purified T cells (anti-mmunoglobulin plate depletion of B cells); (ii) it expressed no known antigenic markers of immunoglobulins (enzyme-linked immunosorbant direct binding assay); (iii) it had a molecular weight of 70,000 or less (sucrose gradient ultracentrifugation); and (iv) it had serological markers associated with antigen-specific T cell factors from other experimental systems. We suggest that, at sites of delayed-type hypersensitivity, antigen-reactive T cells may release antigen-specific factors that lead to mast cell activation and release of vasoactive amines, which is required for elicitation for these responses.The immune response that takes place in the skin of antigenchallenged sensitized subjects has been divided into major classes by virtue of the time it takes for a detectable reaction to appear after the antigenic challenge. On one end of the scale are immediate hypersensitivity reactions, which have been shown to be due to the rapid release of vasoactive amines and other mediators from degranulated mast cells that have been passively sensitized with specific antibody of the IgE isotype (1-3). On the other end of the spectrum are cell-mediated hypersensitivity reactions, in which antigen-specific immune Lyl T cells recruit other inflammatory cells to the site ofthe antigen (4). In this case the series of events that take place before a visible or measurable reaction appears usually requires about 24 hr. Thus these latter reactions have been called delayed-type hypersensitivity. Conventional immunological dogma separates immediate and delayed-type hypersensitivity reactions from one another and implies that they are unrelated.However, some recent experiments suggest that this dogma might need modification. In particular, it has been shown that inhibition ofthe release ofvasoactive amines from mast cells can inhibit both immediate and delayed-type hypersensitivity (5) and that T-cell dependent degranulation of mast cells occurs in delayed-type hypersensitivity (6). These findings in murine models have been interpreted to mean that both the proteinrich fluids that exude from local blood vessels in immediate hypersensitivity and the inflammatory-cells that migrate from the blood to the site of delayed-type hypersensitivity require that vasoactive amines produce gaps between endothelial cells so that the relevant molecules, cells, or both respons...

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mentioning

confidence: 99%

Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

Ptak¹,

Askenase²,

Rosenstein³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…In the last few decades, it has becoming increasingly evident that the prevalence of allergic diseases like allergic rhinoconjunctivitis, atopic asthma and atopic dermatitis has increased, ranging between 10 and 20% of the general population [ 1–3]. The chain of events that lead to the allergic immune response includes the recognition of allergen by the antigen‐presenting cell (APC), antigen presentation to T cells, the production of cytokines like interleukin (IL) ‐4 and IL‐13 by T cells, the synthesis of immunoglobulin (Ig) E by B cells, binding of the IgE to the high affinity IgE receptor (FcεRI) on the surface of mast cells, and on subsequent exposure to the allergen, the cross‐linking of the bound IgE–FcεRI complex with multivalent allergen resulting in the release of chemical mediators like histamine, leukotrienes and prostaglandins [ 4–7]. This immediate phase allergic reaction occurs within several seconds to few minutes upon encounter with antigen and the central cell in this response is the mast cell ( Fig.…”

Section: Discussionmentioning

confidence: 99%

γδ T cells in allergic airway diseases

Pawankar

2000

Clin Experimental Allergy

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Allergic diseases like atopic rhinitis, bronchial asthma and urticaria are prevalent and on the rise. T cells are known to play a fundamental role in allergic diseases through the recognition of antigen, and secretion of TH2-type cytokines like interleukins (IL) -4, -5 and -13, that not only induce the synthesis of IgE but also recruit effector cells like eosinophils and basophils into the site of allergic in¯ammation. Yet, not much has been learnt about the character of these allergen-speci®c T cells, in the target organ. Again, recent studies have suggested that in addition to the ab T-cell receptor (TCR) -bearing cells, the less common gd TCR bearing cells may play important roles in the development and perpetuation of allergic in¯ammation as effector and immunoregulatory cells. The present review focuses on the characteristics and roles of gd T cells in atopic rhinitis and asthma.In the last few decades, it has becoming increasingly evident that the prevalence of allergic diseases like allergic rhinoconjunctivitis, atopic asthma and atopic dermatitis has increased, ranging between 10 and 20% of the general population [1±3]. The chain of events that lead to the allergic immune response includes the recognition of allergen by the antigen-presenting cell (APC), antigen presentation to T cells, the production of cytokines like interleukin (IL) -4 and IL-13 by T cells, the synthesis of immunoglobulin (Ig) E by B cells, binding of the IgE to the high af®nity IgE receptor (FceRI) on the surface of mast cells, and on subsequent exposure to the allergen, the crosslinking of the bound IgE±FceRI complex with multivalent allergen resulting in the release of chemical mediators like histamine, leukotrienes and prostaglandins [4±7]. This immediate phase allergic reaction occurs within several seconds to few minutes upon encounter with antigen and the central cell in this response is the mast cell ( Fig. 1). This is followed by the late phase allergic reaction which occurs after 4±6 h with a recurrence of symptoms that persists for about 24 h. The late phase allergic reaction is largely in¯ammatory and is orchestrated by cytokines released from T lymphocytes. The T-cell-derived cytokines upregulate the expression of adhesion molecules like VCAM-1 and ICAM-1 on endothelial cells, resulting in the in®ltration of eosinophils, and basophils which subsequently release a number of soluble products like prostaglandins, leukotrienes, PAF, ECP and MBP [8,9] (Fig. 1).The reason why only a proportion of individuals develop allergic disease is not yet well understood. An increase in the level of speci®c IgE is a hallmark of atopic diseases, but the genetic basis for this is as yet unknown. Studies on the major histocompatibility complex (MHC) speci®city of allergen-speci®c T cells are limited and population studies of inheritance of atopic disorders do not suggest a dominant role for HLA genes. There is increasing evidence of a link between environmental factors like air pollution (nitrogen oxides, ozone, volatile organic compounds, etc...

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“…Cross‐linking of allergen‐specific IgE bound to the high‐affinity IgE receptor expressed on the surface of mast cells with multivalent antigen results in the release of inflammatory mediators, such as histamine, leukotrienes and prostaglandins etc., 1–4 and in the clinical expression of allergic disease. Seasonal allergic rhinitis (SAR) to Japanese cedar pollen is a prototype of a type I allergic disease that affects approximately 10–20% of the general population in Japan.…”

Section: Introductionmentioning

confidence: 99%

Effect of modified immunotherapy with an allergen–pullulan conjugate in patients with Japanese cedar pollinosis

Pawankar

Takizawa

Goto

et al. 2001

Allergology International

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Immunologic mechanisms of allergen immunotherapy are still incompletely understood. Immunotherapy of a higher maximum tolerance dose with reduced risks of systemic reactions, such as anaphylaxis, needs to be developed. Seasonal allergic rhinitis (SAR) is a type I allergic disease characterized by typical seasonal symptoms of rhinitis and an increase in mast cells and T helper (Th) 2‐type cells, as well as tissue eosinophilia. The present study was designed to investigate the effect of a modified immunotherapy (IT) with an allergen–pullulan conjugate (CS‐560) in patients with SAR to Japanese cedar pollen (Japanese cedar pollinosis) using objective parameters, such as analyzing the alteration in the proportion of effector cells like mast cells, eosinophils and T cells, and the Th2 and Th1 cytokine profile. We also analyzed the efficacy of modified IT on the severity of symptoms, using subjective parameters, such as the symptom–medication score. Immunotherapy for 15 months duration with the modified drug CS‐560 in patients with Japanese cedar pollinosis induced an immune deviation from a Th2‐ to a Th1‐type cytokine profile and inhibited the in‐season increase in the proportion of intraepithelial mast cells and eosinophils. These changes were associated with a reduction in the symptom–medication score. These data suggest that this modified IT with an allergen– pullulan conjugate (CS‐560) is an effective mode of treatment of patients with Japanese cedar pollinosis.

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Immunoglobulin E: Biosynthesis and Immunological Mechanisms of IgE-Mediated Hypersensitivity

Cited by 10 publications

References 64 publications

Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

Transfer of an antigen-specific immediate hypersensitivity-like reaction with an antigen-binding factor produced by T cells.

γδ T cells in allergic airway diseases

Effect of modified immunotherapy with an allergen–pullulan conjugate in patients with Japanese cedar pollinosis

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