Desensitization of IL-4 secretion from mouse bone marrow-derived mast cells

Morihiko Nakamura, Donald Macglashan

Research output: Contribution to journalArticle

Abstract

Several recent findings indicate that mouse bone marrow-derived mast cells (BMMC) express RNA encoding interleukin-4 (IL-4) and secrete detectable amounts of IL-4 in response to cross-linking of Fcε{lunate}RI receptors, FcγR receptors, or to ionomycin. We investigated the desensitization of BMMC from the view point of both IL-4 secretion and histamine release. In a desensitization protocol, the cells were challenged with an optimal concentration of antigen (10 ng/ml of DNP33BSA) in the absence of calcium for various periods of time followed by addition of calcium to determine the loss in ability to release histamine or IL-4. In the context of histamine release, BMMC were desensitized completely in 45 min (T 1 2 ≈ 5 min). By contrast, in the context of IL-4 secretion, BMMC were only partly desensitized (52 ± 5% of the control response) after 1 h of desensitization. A longer-term (2-6 h) desensitization of BMMC did not result in complete inhibition of IL-4 secretion (44 ± 5% of control after 6 h). Northern blot analysis showed that IL-4 mRNA accumulation was decreased after a 1 h desensitization (37% ± 14% of non-desensitized cells), suggesting that desensitization of IL-4 release results from a decrease in the amount of mRNA accumulation. These and other data support the view that the IgE-mediated signal transduction cascade has meditor-specific pathways that are independently regulated by homeostatic mechanisms within mast cells.

Original languageEnglish (US)
Pages (from-to)129-133
Number of pages5
JournalImmunology Letters
Volume41
Issue number2-3
DOIs
StatePublished - 1994

Fingerprint

Mast Cells
Interleukin-4
Bone Marrow
Histamine Release
Calcium
Messenger RNA
Ionomycin
Northern Blotting
Immunoglobulin E
Signal Transduction
RNA
Antigens

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Desensitization of IL-4 secretion from mouse bone marrow-derived mast cells. / Nakamura, Morihiko; Macglashan, Donald.

In: Immunology Letters, Vol. 41, No. 2-3, 1994, p. 129-133.

Research output: Contribution to journalArticle

@article{8e0f28969d514c21abbdefbadf311f08,
title = "Desensitization of IL-4 secretion from mouse bone marrow-derived mast cells",
abstract = "Several recent findings indicate that mouse bone marrow-derived mast cells (BMMC) express RNA encoding interleukin-4 (IL-4) and secrete detectable amounts of IL-4 in response to cross-linking of Fcε{lunate}RI receptors, FcγR receptors, or to ionomycin. We investigated the desensitization of BMMC from the view point of both IL-4 secretion and histamine release. In a desensitization protocol, the cells were challenged with an optimal concentration of antigen (10 ng/ml of DNP33BSA) in the absence of calcium for various periods of time followed by addition of calcium to determine the loss in ability to release histamine or IL-4. In the context of histamine release, BMMC were desensitized completely in 45 min (T 1 2 ≈ 5 min). By contrast, in the context of IL-4 secretion, BMMC were only partly desensitized (52 ± 5{\%} of the control response) after 1 h of desensitization. A longer-term (2-6 h) desensitization of BMMC did not result in complete inhibition of IL-4 secretion (44 ± 5{\%} of control after 6 h). Northern blot analysis showed that IL-4 mRNA accumulation was decreased after a 1 h desensitization (37{\%} ± 14{\%} of non-desensitized cells), suggesting that desensitization of IL-4 release results from a decrease in the amount of mRNA accumulation. These and other data support the view that the IgE-mediated signal transduction cascade has meditor-specific pathways that are independently regulated by homeostatic mechanisms within mast cells.",
author = "Morihiko Nakamura and Donald Macglashan",
year = "1994",
doi = "10.1016/0165-2478(94)90122-8",
language = "English (US)",
volume = "41",
pages = "129--133",
journal = "Immunology Letters",
issn = "0165-2478",
publisher = "Elsevier",
number = "2-3",

}

TY - JOUR

T1 - Desensitization of IL-4 secretion from mouse bone marrow-derived mast cells

AU - Nakamura, Morihiko

AU - Macglashan, Donald

PY - 1994

Y1 - 1994

N2 - Several recent findings indicate that mouse bone marrow-derived mast cells (BMMC) express RNA encoding interleukin-4 (IL-4) and secrete detectable amounts of IL-4 in response to cross-linking of Fcε{lunate}RI receptors, FcγR receptors, or to ionomycin. We investigated the desensitization of BMMC from the view point of both IL-4 secretion and histamine release. In a desensitization protocol, the cells were challenged with an optimal concentration of antigen (10 ng/ml of DNP33BSA) in the absence of calcium for various periods of time followed by addition of calcium to determine the loss in ability to release histamine or IL-4. In the context of histamine release, BMMC were desensitized completely in 45 min (T 1 2 ≈ 5 min). By contrast, in the context of IL-4 secretion, BMMC were only partly desensitized (52 ± 5% of the control response) after 1 h of desensitization. A longer-term (2-6 h) desensitization of BMMC did not result in complete inhibition of IL-4 secretion (44 ± 5% of control after 6 h). Northern blot analysis showed that IL-4 mRNA accumulation was decreased after a 1 h desensitization (37% ± 14% of non-desensitized cells), suggesting that desensitization of IL-4 release results from a decrease in the amount of mRNA accumulation. These and other data support the view that the IgE-mediated signal transduction cascade has meditor-specific pathways that are independently regulated by homeostatic mechanisms within mast cells.

AB - Several recent findings indicate that mouse bone marrow-derived mast cells (BMMC) express RNA encoding interleukin-4 (IL-4) and secrete detectable amounts of IL-4 in response to cross-linking of Fcε{lunate}RI receptors, FcγR receptors, or to ionomycin. We investigated the desensitization of BMMC from the view point of both IL-4 secretion and histamine release. In a desensitization protocol, the cells were challenged with an optimal concentration of antigen (10 ng/ml of DNP33BSA) in the absence of calcium for various periods of time followed by addition of calcium to determine the loss in ability to release histamine or IL-4. In the context of histamine release, BMMC were desensitized completely in 45 min (T 1 2 ≈ 5 min). By contrast, in the context of IL-4 secretion, BMMC were only partly desensitized (52 ± 5% of the control response) after 1 h of desensitization. A longer-term (2-6 h) desensitization of BMMC did not result in complete inhibition of IL-4 secretion (44 ± 5% of control after 6 h). Northern blot analysis showed that IL-4 mRNA accumulation was decreased after a 1 h desensitization (37% ± 14% of non-desensitized cells), suggesting that desensitization of IL-4 release results from a decrease in the amount of mRNA accumulation. These and other data support the view that the IgE-mediated signal transduction cascade has meditor-specific pathways that are independently regulated by homeostatic mechanisms within mast cells.

UR - http://www.scopus.com/inward/record.url?scp=0028088206&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028088206&partnerID=8YFLogxK

U2 - 10.1016/0165-2478(94)90122-8

DO - 10.1016/0165-2478(94)90122-8

M3 - Article

C2 - 7528170

AN - SCOPUS:0028088206

VL - 41

SP - 129

EP - 133

JO - Immunology Letters

JF - Immunology Letters

SN - 0165-2478

IS - 2-3

ER -