Immunoglobulin E (Reagin) and Allergy

Dr, Stanworth

doi:10.1038/233310a0

Cited by 46 publications

(15 citation statements)

References 35 publications

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“…In reactions of this type, antibody (usually IgE) attaches itself to the mast cell via membrane receptors in such a manner that the Fab part of the antibody is left free for union with antigen, a union which results in mast cell degranulation (Stanworth, 1971). That a reaction of this type is occurring in Crohn's disease is suggested by the decrease in IgE-containing immunocytes in the bowel of patients with this disease; this decrease was not simply a dilution effect due to the local oedema, for the overall number of immunocytes was only moderately reduced and not in any way comparable with the marked decline in the IgE-immunocyte population.…”

Section: Discussionmentioning

confidence: 99%

“…In both these diseases, however, the inflammatory lesions are of a mixed type and features of an acute and a chronic inflammatory reaction are often both present. McGovern and Archer (1957) were the first to suggest that the acute inflammatory component of ulcerative colitis was mediated by mast cells, and subsequent workers have claimed that a marked increase in intestinal mast cells is a prominent feature of inflammatory bowel disease, some noting this increase only in ulcerative colitis (McAuley and Sommers, 1961;Bercovitz and Sommers, 1966;Sommers, 1966) and others finding it to be also a feature of Crohn's disease (Hiatt and Katz, 1962 These studies were made at a time when it was not yet fully established that mast cells could react with antigen and IgE to produce an immediate hypersensitivity reaction (Stanworth, 1971). Thus the possibility exists that one of the immunological mechanisms involved in inflammatory bowel disease is an immediate hypersensitivity reaction and it was with this in mind that the mast cell and IgE-containing immunocyte populations of the normal and inflamed bowel were studied.…”

mentioning

confidence: 99%

“…These studies were made at a time when it was not yet fully established that mast cells could react with antigen and IgE to produce an immediate hypersensitivity reaction (Stanworth, 1971). Thus the possibility exists that one of the immunological mechanisms involved in inflammatory bowel disease is an immediate hypersensitivity reaction and it was with this in mind that the mast cell and IgE-containing immunocyte populations of the normal and inflamed bowel were studied.…”

mentioning

confidence: 99%

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Mast cells and immunoglobulin E in inflammatory bowel disease.

Lloyd¹,

Green²,

Fox³

et al. 1975

Gut

108

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It is currently thought that both ulcerative colitis and Crohn's disease may be immunologically mediated, though the exact mechanisms responsible for both initiating and maintaining these two inflammatory bowel conditions are still far from clear. In recent years, the limited role of humoral antibodies in these diseases has become increasingly apparent and interest has tended to centre upon the possibility that they are the result of a cell mediated delayed hypersensitivity type of reaction in the bowel wall. In both these diseases, however, the inflammatory lesions are of a mixed type and features of an acute and a chronic inflammatory reaction are often both present. McGovern and Archer (1957) were the first to suggest that the acute inflammatory component of ulcerative colitis was mediated by mast cells, and subsequent workers have claimed that a marked increase in intestinal mast cells is a prominent feature of inflammatory bowel disease, some noting this increase only in ulcerative colitis (McAuley and Sommers, 1961;Bercovitz and Sommers, 1966;Sommers, 1966) and others finding it to be also a feature of Crohn's disease (Hiatt and Katz, 1962 These studies were made at a time when it was not yet fully established that mast cells could react with antigen and IgE to produce an immediate hypersensitivity reaction (Stanworth, 1971). Thus the possibility exists that one of the immunological mechanisms involved in inflammatory bowel disease is an immediate hypersensitivity reaction and it was with this in mind that the mast cell and IgE-containing immunocyte populations of the normal and inflamed bowel were studied. Methods MAST CELLSA preliminary study showed that bowel obtained at necropsy was unsuitable for the demonstration of mast cells and their distribution was therefore studied in surgically resected or biopsy specimens, all of which were obtained fresh. Thirty specimens of ileum were studied of which 12 were from patients with proven Crohn's disease; the remaining 18 were considered as normal controls and were attached to right hemicolectomy specimens resected for colonic carcinoma. Mast cell distribution was also studied in 44 surgically resected colons and in 60 specimens of rectum, some surgically resected and others obtained at biopsy. Of the colonic specimens, 15 were from patients with Crohn's disease, and 14 from cases of ulcerative colitis; multiple sections were taken from 861 on 11 May 2018 by guest. Protected by copyright.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Mast cells and immunoglobulin E in inflammatory bowel disease.

Lloyd¹,

Green²,

Fox³

et al. 1975

Gut

108

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“…3B in orange) has already been described and characterized earlier (31,32). The authors proposed that this region within C⑀4 might be involved in mast cell triggering (33). This hypothesis gained some support by that fact, that a serum generated against this decapeptide of IgE-C⑀4 inhibited histamine release from rat mast cells (34).…”

Section: Discussionmentioning

confidence: 65%

Molecular Basis for Nonanaphylactogenicity of a Monoclonal Anti-IgE Antibody

Rudolf

Zuercher

Nechansky

et al. 2000

The Journal of Immunology

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IgE Abs mediate allergic responses by binding to specific high affinity receptors (FcεRI) on mast cells and basophils. Therefore, the IgE/FcεRI interaction is a target for clinical intervention in allergic disease. An anti-IgE mAb, termed BSW17, is nonanaphylactogenic, although recognizing IgE bound to FcεRI, and interferes with binding of IgE to FcεRI. Thus, BSW17 represents a candidate Ab for treatment of IgE-mediated disorders. By panning BSW17 against random peptide libraries displayed on phages, we defined mimotopes that mimic the conformational epitope recognized on human IgE. Two types of mimotopes, one within the Cε3 and one within the Cε4 domain, were identified, indicating that this mAb may recognize either a large conformational epitope or eventually two distinct epitopes on IgE. On the basis of alignments of the two mimotopes with the human IgE sequence, we postulate that binding of BSW17 to the Cε3 region predominantly blocks binding of IgE to FcεRI, leading to neutralization of IgE. Moreover, binding of BSW17 to the Cε4 region may explain how BSW17 recognizes FcεRI-bound IgE, and binding to this region may also interfere with degranulation of IgE sensitized cells (basophils and mast cells). As a practical application of these findings, mimotope peptides coupled to a carrier protein may be used for the development of a peptide-based anti–allergy vaccine by induction of anti-IgE Abs similar to the current approach of using humanized nonanaphylactogenic anti-IgE Abs as a passive vaccine.

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“…Thus, as predicted in 1971 (22), the availability of relatively huge quantities of a monoclonal (paraprotein) form, followed later by the discovery of additional IgE myeloma proteins in other parts of the world and their in vitro production by cultured B-cell lines, has (as in the earfier case of the availability of myeloma proteins of the other immunoglobulin classes) provided the key to the complete primary structural analysis of the reaginic antibody. More recently, the use of synthetic peptides representative of various IgE Ec sequences and antibodies against these as structural probes is beginning to reveal important new insights into the molecular pathology of this intriguing immunoglobulin (3,4,24,26).…”

Section: Resultsmentioning

confidence: 99%