Expression of the HML-1 epitope on human monocytes is independent of αE integrin mRNA

Lisa Miller, Congfen Li, Dallas M. Hyde

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Interferon gamma (IFNγ)-mediated activation of the myelomonocytic cell line HL-60 and peripheral blood monocytes will induce expression of an epitope for the monoclonal antibody which recognizes human αEβ7 integrin, HML-1. Here, we found that the anti-human αEβ7 monoclonal antibody Ber-ACT8 did not recognize IFNγ-stimulated, HML-1 positive HL-60 cells. Culture of blood monocytes with IFNγ also induced expression of HML-1 but not Ber-ACT8 epitopes. Moreover, migration of monocytes across a monolayer of human airway epithelial cells rapidly induced expression of HML-1, with no detectable Ber- ACT8 staining. Using two different sets of primers specific for the human αE integrin gene, we were unable to detect αE mRNA within HL-60 cells or isolated monocytes by reverse transcriptase polymerase chain reaction methods. We conclude that reactivity of the HML-1 antibody for HL-60 cells and monocytes does not correspond with the expression of the αE integrin subunit, and instead detects a marker for cellular activation.

Original languageEnglish (US)
Pages (from-to)195-205
Number of pages11
JournalInflammation
Volume24
Issue number3
DOIs
StatePublished - 2000
Externally publishedYes

Fingerprint

Integrins
Epitopes
Monocytes
HL-60 Cells
Messenger RNA
Interferon-gamma
Monoclonal Antibodies
Reverse Transcriptase Polymerase Chain Reaction
Epithelial Cells
Staining and Labeling
Cell Line
Antibodies
Genes

ASJC Scopus subject areas

  • Cell Biology
  • Immunology
  • Medicine(all)

Cite this

Expression of the HML-1 epitope on human monocytes is independent of αE integrin mRNA. / Miller, Lisa; Li, Congfen; Hyde, Dallas M.

In: Inflammation, Vol. 24, No. 3, 2000, p. 195-205.

Research output: Contribution to journalArticle

Miller, Lisa ; Li, Congfen ; Hyde, Dallas M. / Expression of the HML-1 epitope on human monocytes is independent of αE integrin mRNA. In: Inflammation. 2000 ; Vol. 24, No. 3. pp. 195-205.
@article{4a9872c820e14095b57e705a0c884bf8,
title = "Expression of the HML-1 epitope on human monocytes is independent of αE integrin mRNA",
abstract = "Interferon gamma (IFNγ)-mediated activation of the myelomonocytic cell line HL-60 and peripheral blood monocytes will induce expression of an epitope for the monoclonal antibody which recognizes human αEβ7 integrin, HML-1. Here, we found that the anti-human αEβ7 monoclonal antibody Ber-ACT8 did not recognize IFNγ-stimulated, HML-1 positive HL-60 cells. Culture of blood monocytes with IFNγ also induced expression of HML-1 but not Ber-ACT8 epitopes. Moreover, migration of monocytes across a monolayer of human airway epithelial cells rapidly induced expression of HML-1, with no detectable Ber- ACT8 staining. Using two different sets of primers specific for the human αE integrin gene, we were unable to detect αE mRNA within HL-60 cells or isolated monocytes by reverse transcriptase polymerase chain reaction methods. We conclude that reactivity of the HML-1 antibody for HL-60 cells and monocytes does not correspond with the expression of the αE integrin subunit, and instead detects a marker for cellular activation.",
author = "Lisa Miller and Congfen Li and Hyde, {Dallas M.}",
year = "2000",
doi = "10.1023/A:1007007428255",
language = "English (US)",
volume = "24",
pages = "195--205",
journal = "Inflammation",
issn = "0360-3997",
publisher = "Springer New York",
number = "3",

}

TY - JOUR

T1 - Expression of the HML-1 epitope on human monocytes is independent of αE integrin mRNA

AU - Miller, Lisa

AU - Li, Congfen

AU - Hyde, Dallas M.

PY - 2000

Y1 - 2000

N2 - Interferon gamma (IFNγ)-mediated activation of the myelomonocytic cell line HL-60 and peripheral blood monocytes will induce expression of an epitope for the monoclonal antibody which recognizes human αEβ7 integrin, HML-1. Here, we found that the anti-human αEβ7 monoclonal antibody Ber-ACT8 did not recognize IFNγ-stimulated, HML-1 positive HL-60 cells. Culture of blood monocytes with IFNγ also induced expression of HML-1 but not Ber-ACT8 epitopes. Moreover, migration of monocytes across a monolayer of human airway epithelial cells rapidly induced expression of HML-1, with no detectable Ber- ACT8 staining. Using two different sets of primers specific for the human αE integrin gene, we were unable to detect αE mRNA within HL-60 cells or isolated monocytes by reverse transcriptase polymerase chain reaction methods. We conclude that reactivity of the HML-1 antibody for HL-60 cells and monocytes does not correspond with the expression of the αE integrin subunit, and instead detects a marker for cellular activation.

AB - Interferon gamma (IFNγ)-mediated activation of the myelomonocytic cell line HL-60 and peripheral blood monocytes will induce expression of an epitope for the monoclonal antibody which recognizes human αEβ7 integrin, HML-1. Here, we found that the anti-human αEβ7 monoclonal antibody Ber-ACT8 did not recognize IFNγ-stimulated, HML-1 positive HL-60 cells. Culture of blood monocytes with IFNγ also induced expression of HML-1 but not Ber-ACT8 epitopes. Moreover, migration of monocytes across a monolayer of human airway epithelial cells rapidly induced expression of HML-1, with no detectable Ber- ACT8 staining. Using two different sets of primers specific for the human αE integrin gene, we were unable to detect αE mRNA within HL-60 cells or isolated monocytes by reverse transcriptase polymerase chain reaction methods. We conclude that reactivity of the HML-1 antibody for HL-60 cells and monocytes does not correspond with the expression of the αE integrin subunit, and instead detects a marker for cellular activation.

UR - http://www.scopus.com/inward/record.url?scp=0034005035&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034005035&partnerID=8YFLogxK

U2 - 10.1023/A:1007007428255

DO - 10.1023/A:1007007428255

M3 - Article

AN - SCOPUS:0034005035

VL - 24

SP - 195

EP - 205

JO - Inflammation

JF - Inflammation

SN - 0360-3997

IS - 3

ER -