Repository corticotropin injection reverses critical elements of the TLR9/B cell receptor activation response in human B cells in vitro

Nancy Olsen, Ann L. Benko, Carl A. McAloose, Patrice M. Becker, Dale Wright, Teresa Sunyer, Yuka Imamura, William Kovacs

Research output: Contribution to journalArticle

Abstract

We sought evidence for direct effects of repository corticotropin (RCI; an FDA-approved treatment for selected cases of SLE) on isolated human B lymphocytes activated by engagement of TLR9 and B cell receptors. ODN 2395/αIgM treatment was found to result in induction of 162 distinct mRNAs and suppression of 80 mRNAs at 24 h. RCI treatment resulted in suppression of 14 of the ODN 2395/αIgM -induced mRNAs (mean suppression to 23.6 ± 3.1% of stimulated value). The RCI-suppressed mRNAs included two critical regulators of class switch recombination, AICDA and BATF. RCI treatment also resulted in induction of 5 of the ODN 2395/αIgM -suppressed mRNAs (mean induction by RCI = 7.65 ± 2.34-fold). The RCI-induced mRNAs included SLAMF3, a cell surface receptor capable of inhibiting autoantibody responses. These studies reveal that RCI treatment of human B cells reverses key elements of the early mRNA response to TLR9 and B cell receptor engagement.

Original languageEnglish (US)
Pages (from-to)70-78
Number of pages9
JournalClinical Immunology
Volume201
DOIs
StatePublished - Apr 1 2019

Fingerprint

Adrenocorticotropic Hormone
B-Lymphocytes
Messenger RNA
Injections
Immunoglobulin M
Therapeutics
Cell Surface Receptors
In Vitro Techniques
Autoantibodies
Genetic Recombination

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

@article{7d4cbb059ee54ce68fde554e3a117290,
title = "Repository corticotropin injection reverses critical elements of the TLR9/B cell receptor activation response in human B cells in vitro",
abstract = "We sought evidence for direct effects of repository corticotropin (RCI; an FDA-approved treatment for selected cases of SLE) on isolated human B lymphocytes activated by engagement of TLR9 and B cell receptors. ODN 2395/αIgM treatment was found to result in induction of 162 distinct mRNAs and suppression of 80 mRNAs at 24 h. RCI treatment resulted in suppression of 14 of the ODN 2395/αIgM -induced mRNAs (mean suppression to 23.6 ± 3.1{\%} of stimulated value). The RCI-suppressed mRNAs included two critical regulators of class switch recombination, AICDA and BATF. RCI treatment also resulted in induction of 5 of the ODN 2395/αIgM -suppressed mRNAs (mean induction by RCI = 7.65 ± 2.34-fold). The RCI-induced mRNAs included SLAMF3, a cell surface receptor capable of inhibiting autoantibody responses. These studies reveal that RCI treatment of human B cells reverses key elements of the early mRNA response to TLR9 and B cell receptor engagement.",
author = "Nancy Olsen and Benko, {Ann L.} and McAloose, {Carl A.} and Becker, {Patrice M.} and Dale Wright and Teresa Sunyer and Yuka Imamura and William Kovacs",
year = "2019",
month = "4",
day = "1",
doi = "10.1016/j.clim.2019.02.009",
language = "English (US)",
volume = "201",
pages = "70--78",
journal = "Clinical Immunology",
issn = "1521-6616",
publisher = "Academic Press Inc.",

}

Repository corticotropin injection reverses critical elements of the TLR9/B cell receptor activation response in human B cells in vitro. / Olsen, Nancy; Benko, Ann L.; McAloose, Carl A.; Becker, Patrice M.; Wright, Dale; Sunyer, Teresa; Imamura, Yuka; Kovacs, William.

In: Clinical Immunology, Vol. 201, 01.04.2019, p. 70-78.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Repository corticotropin injection reverses critical elements of the TLR9/B cell receptor activation response in human B cells in vitro

AU - Olsen, Nancy

AU - Benko, Ann L.

AU - McAloose, Carl A.

AU - Becker, Patrice M.

AU - Wright, Dale

AU - Sunyer, Teresa

AU - Imamura, Yuka

AU - Kovacs, William

PY - 2019/4/1

Y1 - 2019/4/1

N2 - We sought evidence for direct effects of repository corticotropin (RCI; an FDA-approved treatment for selected cases of SLE) on isolated human B lymphocytes activated by engagement of TLR9 and B cell receptors. ODN 2395/αIgM treatment was found to result in induction of 162 distinct mRNAs and suppression of 80 mRNAs at 24 h. RCI treatment resulted in suppression of 14 of the ODN 2395/αIgM -induced mRNAs (mean suppression to 23.6 ± 3.1% of stimulated value). The RCI-suppressed mRNAs included two critical regulators of class switch recombination, AICDA and BATF. RCI treatment also resulted in induction of 5 of the ODN 2395/αIgM -suppressed mRNAs (mean induction by RCI = 7.65 ± 2.34-fold). The RCI-induced mRNAs included SLAMF3, a cell surface receptor capable of inhibiting autoantibody responses. These studies reveal that RCI treatment of human B cells reverses key elements of the early mRNA response to TLR9 and B cell receptor engagement.

AB - We sought evidence for direct effects of repository corticotropin (RCI; an FDA-approved treatment for selected cases of SLE) on isolated human B lymphocytes activated by engagement of TLR9 and B cell receptors. ODN 2395/αIgM treatment was found to result in induction of 162 distinct mRNAs and suppression of 80 mRNAs at 24 h. RCI treatment resulted in suppression of 14 of the ODN 2395/αIgM -induced mRNAs (mean suppression to 23.6 ± 3.1% of stimulated value). The RCI-suppressed mRNAs included two critical regulators of class switch recombination, AICDA and BATF. RCI treatment also resulted in induction of 5 of the ODN 2395/αIgM -suppressed mRNAs (mean induction by RCI = 7.65 ± 2.34-fold). The RCI-induced mRNAs included SLAMF3, a cell surface receptor capable of inhibiting autoantibody responses. These studies reveal that RCI treatment of human B cells reverses key elements of the early mRNA response to TLR9 and B cell receptor engagement.

UR - http://www.scopus.com/inward/record.url?scp=85062635229&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85062635229&partnerID=8YFLogxK

U2 - 10.1016/j.clim.2019.02.009

DO - 10.1016/j.clim.2019.02.009

M3 - Article

VL - 201

SP - 70

EP - 78

JO - Clinical Immunology

JF - Clinical Immunology

SN - 1521-6616

ER -