Histamine-releasing factors and inhibitors: Historical perspectives and possible implications in human illness

J. Andrew Grant, Rafeul Alam, Michael A. Lett-Brown

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

The initiation of allergic reactions with the bridging of surface-bound IgE antibodies on mast cells and basophils by allergens is well recognized. However, it is clear that other factors most likely play a role in regulating these cells. A number of cytokines have been identified that modulate the secretory response of mast cells and basophils. Among the well-characterized cytokines, interleukin-3 and connective tissue-activating peptide III (or its degradation product, neutrophil-activating peptide 2) can increase the secretory response, whereas interleukin-8 specifically inhibits the response to cytokines. Additional factors are currently under investigation. Preliminary studies suggest an important role for these histamine-releasing factors in atopic disorders, as well as in other conditions in which an IgE-dependent mechanism is not demonstrable. Furthermore, these cytokines may modulate the response of basophils and mast cells in physiologic conditions, such as tissue repair and host defense.

Original languageEnglish (US)
Pages (from-to)683-693
Number of pages11
JournalThe Journal of Allergy and Clinical Immunology
Volume88
Issue number5
DOIs
StatePublished - 1991

Fingerprint

Basophils
Mast Cells
Cytokines
Immunoglobulin E
Interleukin-3
Interleukin-8
Allergens
Hypersensitivity
translationally-controlled 1 tumor protein
Antibodies
connective tissue-activating peptide

Keywords

  • basophils
  • histamine
  • Histamine-releasing factor
  • hypersensitivity
  • interleukins

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Histamine-releasing factors and inhibitors : Historical perspectives and possible implications in human illness. / Grant, J. Andrew; Alam, Rafeul; Lett-Brown, Michael A.

In: The Journal of Allergy and Clinical Immunology, Vol. 88, No. 5, 1991, p. 683-693.

Research output: Contribution to journalArticle

@article{88691a19ee5c4e3cbf8416c6da51f659,
title = "Histamine-releasing factors and inhibitors: Historical perspectives and possible implications in human illness",
abstract = "The initiation of allergic reactions with the bridging of surface-bound IgE antibodies on mast cells and basophils by allergens is well recognized. However, it is clear that other factors most likely play a role in regulating these cells. A number of cytokines have been identified that modulate the secretory response of mast cells and basophils. Among the well-characterized cytokines, interleukin-3 and connective tissue-activating peptide III (or its degradation product, neutrophil-activating peptide 2) can increase the secretory response, whereas interleukin-8 specifically inhibits the response to cytokines. Additional factors are currently under investigation. Preliminary studies suggest an important role for these histamine-releasing factors in atopic disorders, as well as in other conditions in which an IgE-dependent mechanism is not demonstrable. Furthermore, these cytokines may modulate the response of basophils and mast cells in physiologic conditions, such as tissue repair and host defense.",
keywords = "basophils, histamine, Histamine-releasing factor, hypersensitivity, interleukins",
author = "Grant, {J. Andrew} and Rafeul Alam and Lett-Brown, {Michael A.}",
year = "1991",
doi = "10.1016/0091-6749(91)90170-S",
language = "English (US)",
volume = "88",
pages = "683--693",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "5",

}

TY - JOUR

T1 - Histamine-releasing factors and inhibitors

T2 - Historical perspectives and possible implications in human illness

AU - Grant, J. Andrew

AU - Alam, Rafeul

AU - Lett-Brown, Michael A.

PY - 1991

Y1 - 1991

N2 - The initiation of allergic reactions with the bridging of surface-bound IgE antibodies on mast cells and basophils by allergens is well recognized. However, it is clear that other factors most likely play a role in regulating these cells. A number of cytokines have been identified that modulate the secretory response of mast cells and basophils. Among the well-characterized cytokines, interleukin-3 and connective tissue-activating peptide III (or its degradation product, neutrophil-activating peptide 2) can increase the secretory response, whereas interleukin-8 specifically inhibits the response to cytokines. Additional factors are currently under investigation. Preliminary studies suggest an important role for these histamine-releasing factors in atopic disorders, as well as in other conditions in which an IgE-dependent mechanism is not demonstrable. Furthermore, these cytokines may modulate the response of basophils and mast cells in physiologic conditions, such as tissue repair and host defense.

AB - The initiation of allergic reactions with the bridging of surface-bound IgE antibodies on mast cells and basophils by allergens is well recognized. However, it is clear that other factors most likely play a role in regulating these cells. A number of cytokines have been identified that modulate the secretory response of mast cells and basophils. Among the well-characterized cytokines, interleukin-3 and connective tissue-activating peptide III (or its degradation product, neutrophil-activating peptide 2) can increase the secretory response, whereas interleukin-8 specifically inhibits the response to cytokines. Additional factors are currently under investigation. Preliminary studies suggest an important role for these histamine-releasing factors in atopic disorders, as well as in other conditions in which an IgE-dependent mechanism is not demonstrable. Furthermore, these cytokines may modulate the response of basophils and mast cells in physiologic conditions, such as tissue repair and host defense.

KW - basophils

KW - histamine

KW - Histamine-releasing factor

KW - hypersensitivity

KW - interleukins

UR - http://www.scopus.com/inward/record.url?scp=0026331605&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026331605&partnerID=8YFLogxK

U2 - 10.1016/0091-6749(91)90170-S

DO - 10.1016/0091-6749(91)90170-S

M3 - Article

C2 - 1720148

AN - SCOPUS:0026331605

VL - 88

SP - 683

EP - 693

JO - Journal of Allergy and Clinical Immunology

JF - Journal of Allergy and Clinical Immunology

SN - 0091-6749

IS - 5

ER -