Atopy as a minimal immunodeficiency?

G. R. Burgio, L. Nespoli, A. G. Ugazio

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective "immune exclusion" by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.

Original languageEnglish
Pages (from-to)221-229
Number of pages9
JournalEuropean Journal of Pediatrics
Volume129
Issue number4
DOIs
Publication statusPublished - Dec 1978

Fingerprint

IgA Deficiency
Wiskott-Aldrich Syndrome
Immune System

Keywords

  • Atopy
  • IgA deficiency
  • Immunodeficiency
  • Immunoglobulin E

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Burgio, G. R., Nespoli, L., & Ugazio, A. G. (1978). Atopy as a minimal immunodeficiency? European Journal of Pediatrics, 129(4), 221-229. https://doi.org/10.1007/BF00441353

Atopy as a minimal immunodeficiency? / Burgio, G. R.; Nespoli, L.; Ugazio, A. G.

In: European Journal of Pediatrics, Vol. 129, No. 4, 12.1978, p. 221-229.

Research output: Contribution to journalArticle

Burgio, GR, Nespoli, L & Ugazio, AG 1978, 'Atopy as a minimal immunodeficiency?', European Journal of Pediatrics, vol. 129, no. 4, pp. 221-229. https://doi.org/10.1007/BF00441353
Burgio, G. R. ; Nespoli, L. ; Ugazio, A. G. / Atopy as a minimal immunodeficiency?. In: European Journal of Pediatrics. 1978 ; Vol. 129, No. 4. pp. 221-229.
@article{0a8fb08704534661a3a4bcd5dca5d6ba,
title = "Atopy as a minimal immunodeficiency?",
abstract = "Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective {"}immune exclusion{"} by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.",
keywords = "Atopy, IgA deficiency, Immunodeficiency, Immunoglobulin E",
author = "Burgio, {G. R.} and L. Nespoli and Ugazio, {A. G.}",
year = "1978",
month = "12",
doi = "10.1007/BF00441353",
language = "English",
volume = "129",
pages = "221--229",
journal = "European Journal of Pediatrics",
issn = "0340-6199",
publisher = "Springer Berlin Heidelberg",
number = "4",

}

TY - JOUR

T1 - Atopy as a minimal immunodeficiency?

AU - Burgio, G. R.

AU - Nespoli, L.

AU - Ugazio, A. G.

PY - 1978/12

Y1 - 1978/12

N2 - Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective "immune exclusion" by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.

AB - Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective "immune exclusion" by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.

KW - Atopy

KW - IgA deficiency

KW - Immunodeficiency

KW - Immunoglobulin E

UR - http://www.scopus.com/inward/record.url?scp=0018117490&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018117490&partnerID=8YFLogxK

U2 - 10.1007/BF00441353

DO - 10.1007/BF00441353

M3 - Article

VL - 129

SP - 221

EP - 229

JO - European Journal of Pediatrics

JF - European Journal of Pediatrics

SN - 0340-6199

IS - 4

ER -