Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin

Rahul D. Pawar, Beatrice Goilav, Yumin Xia, Haoyang Zhuang, Leal Herlitz, Westley H. Reeves, Chaim Putterman

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The onset of autoantibodies in systemic autoimmunity can be the result of a breakdown in tolerance at multiple checkpoints. Genetic, hormonal, and immunological factors can combine with environmental influences to accelerate the onset of disease and aggravate disease outcome. Here, we describe a novel mechanism relating to the regulatory role of Neutrophil Gelatinase Associated Lipocalin (NGAL) in modulating the levels of autoantibodies in pristane induced lupus. Following a single injection of pristane intraperitoneally, NGAL expression was induced in both the serum and spleen. Furthermore, NGAL deficient mice were more susceptible to the induction of pristane stimulated autoimmunity, and displayed higher numbers of autoantibody secreting cells and increased expression of activation induced cytidine deaminase (AID) and other inflammatory mediators in the spleen. In contrast, kidney damage was milder in NGAL deficient mice, indicating that NGAL was detrimental in autoantibody mediated kidney disease. These studies indicate that NGAL plays differential roles in different tissues in the context of lupus, and suggest a previously unrecognized role for NGAL in adaptive immunity.

Original languageEnglish (US)
Pages (from-to)49-65
Number of pages17
JournalClinical Immunology
Volume154
Issue number1
DOIs
StatePublished - 2014

Fingerprint

Autoantibodies
Serum
Autoimmunity
Spleen
Immunologic Factors
Kidney Diseases
Adaptive Immunity
pristane
Lipocalin-2
Kidney
Injections

Keywords

  • Autoantibodies
  • Lipocalin-2
  • NGAL
  • Pristane
  • SLE

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin. / Pawar, Rahul D.; Goilav, Beatrice; Xia, Yumin; Zhuang, Haoyang; Herlitz, Leal; Reeves, Westley H.; Putterman, Chaim.

In: Clinical Immunology, Vol. 154, No. 1, 2014, p. 49-65.

Research output: Contribution to journalArticle

Pawar, Rahul D. ; Goilav, Beatrice ; Xia, Yumin ; Zhuang, Haoyang ; Herlitz, Leal ; Reeves, Westley H. ; Putterman, Chaim. / Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin. In: Clinical Immunology. 2014 ; Vol. 154, No. 1. pp. 49-65.
@article{f1fe01e9cb84424db352296b45c848ea,
title = "Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin",
abstract = "The onset of autoantibodies in systemic autoimmunity can be the result of a breakdown in tolerance at multiple checkpoints. Genetic, hormonal, and immunological factors can combine with environmental influences to accelerate the onset of disease and aggravate disease outcome. Here, we describe a novel mechanism relating to the regulatory role of Neutrophil Gelatinase Associated Lipocalin (NGAL) in modulating the levels of autoantibodies in pristane induced lupus. Following a single injection of pristane intraperitoneally, NGAL expression was induced in both the serum and spleen. Furthermore, NGAL deficient mice were more susceptible to the induction of pristane stimulated autoimmunity, and displayed higher numbers of autoantibody secreting cells and increased expression of activation induced cytidine deaminase (AID) and other inflammatory mediators in the spleen. In contrast, kidney damage was milder in NGAL deficient mice, indicating that NGAL was detrimental in autoantibody mediated kidney disease. These studies indicate that NGAL plays differential roles in different tissues in the context of lupus, and suggest a previously unrecognized role for NGAL in adaptive immunity.",
keywords = "Autoantibodies, Lipocalin-2, NGAL, Pristane, SLE",
author = "Pawar, {Rahul D.} and Beatrice Goilav and Yumin Xia and Haoyang Zhuang and Leal Herlitz and Reeves, {Westley H.} and Chaim Putterman",
year = "2014",
doi = "10.1016/j.clim.2014.06.007",
language = "English (US)",
volume = "154",
pages = "49--65",
journal = "Clinical Immunology",
issn = "1521-6616",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Serum autoantibodies in pristane induced lupus are regulated by neutrophil gelatinase associated lipocalin

AU - Pawar, Rahul D.

AU - Goilav, Beatrice

AU - Xia, Yumin

AU - Zhuang, Haoyang

AU - Herlitz, Leal

AU - Reeves, Westley H.

AU - Putterman, Chaim

PY - 2014

Y1 - 2014

N2 - The onset of autoantibodies in systemic autoimmunity can be the result of a breakdown in tolerance at multiple checkpoints. Genetic, hormonal, and immunological factors can combine with environmental influences to accelerate the onset of disease and aggravate disease outcome. Here, we describe a novel mechanism relating to the regulatory role of Neutrophil Gelatinase Associated Lipocalin (NGAL) in modulating the levels of autoantibodies in pristane induced lupus. Following a single injection of pristane intraperitoneally, NGAL expression was induced in both the serum and spleen. Furthermore, NGAL deficient mice were more susceptible to the induction of pristane stimulated autoimmunity, and displayed higher numbers of autoantibody secreting cells and increased expression of activation induced cytidine deaminase (AID) and other inflammatory mediators in the spleen. In contrast, kidney damage was milder in NGAL deficient mice, indicating that NGAL was detrimental in autoantibody mediated kidney disease. These studies indicate that NGAL plays differential roles in different tissues in the context of lupus, and suggest a previously unrecognized role for NGAL in adaptive immunity.

AB - The onset of autoantibodies in systemic autoimmunity can be the result of a breakdown in tolerance at multiple checkpoints. Genetic, hormonal, and immunological factors can combine with environmental influences to accelerate the onset of disease and aggravate disease outcome. Here, we describe a novel mechanism relating to the regulatory role of Neutrophil Gelatinase Associated Lipocalin (NGAL) in modulating the levels of autoantibodies in pristane induced lupus. Following a single injection of pristane intraperitoneally, NGAL expression was induced in both the serum and spleen. Furthermore, NGAL deficient mice were more susceptible to the induction of pristane stimulated autoimmunity, and displayed higher numbers of autoantibody secreting cells and increased expression of activation induced cytidine deaminase (AID) and other inflammatory mediators in the spleen. In contrast, kidney damage was milder in NGAL deficient mice, indicating that NGAL was detrimental in autoantibody mediated kidney disease. These studies indicate that NGAL plays differential roles in different tissues in the context of lupus, and suggest a previously unrecognized role for NGAL in adaptive immunity.

KW - Autoantibodies

KW - Lipocalin-2

KW - NGAL

KW - Pristane

KW - SLE

UR - http://www.scopus.com/inward/record.url?scp=84903889643&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84903889643&partnerID=8YFLogxK

U2 - 10.1016/j.clim.2014.06.007

DO - 10.1016/j.clim.2014.06.007

M3 - Article

C2 - 24971701

AN - SCOPUS:84903889643

VL - 154

SP - 49

EP - 65

JO - Clinical Immunology

JF - Clinical Immunology

SN - 1521-6616

IS - 1

ER -