Regulation of IgE synthesis

from the membrane to the genes

Donata Vercelli, Raif S. Geha

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

The data discussed above clearly indicate that the second signal(s) required for IgE production can be delivered to B cells through different pathways. At the present time, no unifying explanatory mechanism can reconcile all different observations. Not much is known about signalling via MHC class II molecules and CD40; the role played by hydrocortisone is not clear, and other molecules - in addition to CD40 and its ligand - might be involved in non-cognate T-B cell interactions. Signalling via CD21 is not sufficient for IgE induction, and EBV-induced proteins essential for IgE induction have not been identified. The observation that engagement of CD40 [32] and full expression of latent EBV proteins [21] share the ability to protect human B cells from programmed cell death (apoptosis) is certainly intriguing, but it is unclear whether this effect is in any way related to IgE induction. It seems plausible that the pathways mentioned above may share the ability to activate the switch recombination machinery in B cells in which the e{open} locus has been transcriptionally activated and made accessible by IL-4.

Original languageEnglish (US)
Pages (from-to)5-16
Number of pages12
JournalSpringer Seminars in Immunopathology
Volume15
Issue number1
DOIs
StatePublished - Jun 1993
Externally publishedYes

Fingerprint

Immunoglobulin E
B-Lymphocytes
Membranes
Human Herpesvirus 4
Genes
CD40 Ligand
Cell Communication
Interleukin-4
Genetic Recombination
Hydrocortisone
Proteins
Cell Death
Apoptosis

ASJC Scopus subject areas

  • Immunology

Cite this

Regulation of IgE synthesis : from the membrane to the genes. / Vercelli, Donata; Geha, Raif S.

In: Springer Seminars in Immunopathology, Vol. 15, No. 1, 06.1993, p. 5-16.

Research output: Contribution to journalArticle

@article{5565b13a718949b783c0ef8b19dfe6e8,
title = "Regulation of IgE synthesis: from the membrane to the genes",
abstract = "The data discussed above clearly indicate that the second signal(s) required for IgE production can be delivered to B cells through different pathways. At the present time, no unifying explanatory mechanism can reconcile all different observations. Not much is known about signalling via MHC class II molecules and CD40; the role played by hydrocortisone is not clear, and other molecules - in addition to CD40 and its ligand - might be involved in non-cognate T-B cell interactions. Signalling via CD21 is not sufficient for IgE induction, and EBV-induced proteins essential for IgE induction have not been identified. The observation that engagement of CD40 [32] and full expression of latent EBV proteins [21] share the ability to protect human B cells from programmed cell death (apoptosis) is certainly intriguing, but it is unclear whether this effect is in any way related to IgE induction. It seems plausible that the pathways mentioned above may share the ability to activate the switch recombination machinery in B cells in which the e{open} locus has been transcriptionally activated and made accessible by IL-4.",
author = "Donata Vercelli and Geha, {Raif S.}",
year = "1993",
month = "6",
doi = "10.1007/BF00204622",
language = "English (US)",
volume = "15",
pages = "5--16",
journal = "Seminars in Immunopathology",
issn = "1863-2297",
publisher = "Springer Verlag",
number = "1",

}

TY - JOUR

T1 - Regulation of IgE synthesis

T2 - from the membrane to the genes

AU - Vercelli, Donata

AU - Geha, Raif S.

PY - 1993/6

Y1 - 1993/6

N2 - The data discussed above clearly indicate that the second signal(s) required for IgE production can be delivered to B cells through different pathways. At the present time, no unifying explanatory mechanism can reconcile all different observations. Not much is known about signalling via MHC class II molecules and CD40; the role played by hydrocortisone is not clear, and other molecules - in addition to CD40 and its ligand - might be involved in non-cognate T-B cell interactions. Signalling via CD21 is not sufficient for IgE induction, and EBV-induced proteins essential for IgE induction have not been identified. The observation that engagement of CD40 [32] and full expression of latent EBV proteins [21] share the ability to protect human B cells from programmed cell death (apoptosis) is certainly intriguing, but it is unclear whether this effect is in any way related to IgE induction. It seems plausible that the pathways mentioned above may share the ability to activate the switch recombination machinery in B cells in which the e{open} locus has been transcriptionally activated and made accessible by IL-4.

AB - The data discussed above clearly indicate that the second signal(s) required for IgE production can be delivered to B cells through different pathways. At the present time, no unifying explanatory mechanism can reconcile all different observations. Not much is known about signalling via MHC class II molecules and CD40; the role played by hydrocortisone is not clear, and other molecules - in addition to CD40 and its ligand - might be involved in non-cognate T-B cell interactions. Signalling via CD21 is not sufficient for IgE induction, and EBV-induced proteins essential for IgE induction have not been identified. The observation that engagement of CD40 [32] and full expression of latent EBV proteins [21] share the ability to protect human B cells from programmed cell death (apoptosis) is certainly intriguing, but it is unclear whether this effect is in any way related to IgE induction. It seems plausible that the pathways mentioned above may share the ability to activate the switch recombination machinery in B cells in which the e{open} locus has been transcriptionally activated and made accessible by IL-4.

UR - http://www.scopus.com/inward/record.url?scp=0027212185&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027212185&partnerID=8YFLogxK

U2 - 10.1007/BF00204622

DO - 10.1007/BF00204622

M3 - Article

VL - 15

SP - 5

EP - 16

JO - Seminars in Immunopathology

JF - Seminars in Immunopathology

SN - 1863-2297

IS - 1

ER -