Inhibition of diabetes in NOD mice by idiotypic induction of SLE

I. Krause, Yaron Tomer, D. Elias, M. Blank, B. Gilburd, I. R. Cohen, Y. Shoenfeld

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

The present study was undertaken to investigate whether active induction of systemic lupus erythematosus (SLE) in non-obese diabetic (NOD) mice could affect their development of insulin-dependent diabetes mellitus (IDDM). NOD mice were immunized with a human IgM mAb carrying the 16/6 idiotype (MIV-7) or with control human IgM. The mice were bled monthly and tested for SLE- associated autoantibodies in the serum and for the presence of leukopenia, thrombocytopenia, proteinuria and immunoglobulin deposits in the kidneys. The development of diabetes was determined by a blood glucose level exceeding 15 mM on two consecutive weekly determinations and by the presence of insulitis in the pancreas. The NOD mice immunized with MIV-7 developed high and persistent levels of autoantibodies, including anti-DNA, anti-histones and anti-cardiolipin, untreated mice and those immunized with normal human IgM did not produce these autoantibodies. The MIV-7-immunized mice also manifested an elevated erythrocyte sedimentation rate, leukopenia, thrombocytopenia and significant proteinuria, as well as deposits of Ig in their kidney glomeruli. Thus, NOD mice immunized with MIV-7 developed both autoantibodies and clinical features of SLE. The MIV-7-treated mice, however, showed a significantly lower incidence of IDDM (25% vs. 90%, P

Original languageEnglish (US)
Pages (from-to)49-55
Number of pages7
JournalJournal of Autoimmunity
Volume13
Issue number1
DOIs
StatePublished - Aug 1999
Externally publishedYes

Fingerprint

Inbred NOD Mouse
Systemic Lupus Erythematosus
Autoantibodies
Immunoglobulin M
Leukopenia
Type 1 Diabetes Mellitus
Proteinuria
Thrombocytopenia
Kidney Glomerulus
Cardiolipins
Blood Sedimentation
Histones
Blood Glucose
Immunoglobulins
Pancreas
Kidney
DNA
Incidence
Serum

Keywords

  • Autoantibodies
  • Diabetes
  • Idiotypes
  • NOD
  • SLE

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Krause, I., Tomer, Y., Elias, D., Blank, M., Gilburd, B., Cohen, I. R., & Shoenfeld, Y. (1999). Inhibition of diabetes in NOD mice by idiotypic induction of SLE. Journal of Autoimmunity, 13(1), 49-55. https://doi.org/10.1006/jaut.1999.0292

Inhibition of diabetes in NOD mice by idiotypic induction of SLE. / Krause, I.; Tomer, Yaron; Elias, D.; Blank, M.; Gilburd, B.; Cohen, I. R.; Shoenfeld, Y.

In: Journal of Autoimmunity, Vol. 13, No. 1, 08.1999, p. 49-55.

Research output: Contribution to journalArticle

Krause, I, Tomer, Y, Elias, D, Blank, M, Gilburd, B, Cohen, IR & Shoenfeld, Y 1999, 'Inhibition of diabetes in NOD mice by idiotypic induction of SLE', Journal of Autoimmunity, vol. 13, no. 1, pp. 49-55. https://doi.org/10.1006/jaut.1999.0292
Krause, I. ; Tomer, Yaron ; Elias, D. ; Blank, M. ; Gilburd, B. ; Cohen, I. R. ; Shoenfeld, Y. / Inhibition of diabetes in NOD mice by idiotypic induction of SLE. In: Journal of Autoimmunity. 1999 ; Vol. 13, No. 1. pp. 49-55.
@article{74c58e8ffe7a4563ad22a91068bb659c,
title = "Inhibition of diabetes in NOD mice by idiotypic induction of SLE",
abstract = "The present study was undertaken to investigate whether active induction of systemic lupus erythematosus (SLE) in non-obese diabetic (NOD) mice could affect their development of insulin-dependent diabetes mellitus (IDDM). NOD mice were immunized with a human IgM mAb carrying the 16/6 idiotype (MIV-7) or with control human IgM. The mice were bled monthly and tested for SLE- associated autoantibodies in the serum and for the presence of leukopenia, thrombocytopenia, proteinuria and immunoglobulin deposits in the kidneys. The development of diabetes was determined by a blood glucose level exceeding 15 mM on two consecutive weekly determinations and by the presence of insulitis in the pancreas. The NOD mice immunized with MIV-7 developed high and persistent levels of autoantibodies, including anti-DNA, anti-histones and anti-cardiolipin, untreated mice and those immunized with normal human IgM did not produce these autoantibodies. The MIV-7-immunized mice also manifested an elevated erythrocyte sedimentation rate, leukopenia, thrombocytopenia and significant proteinuria, as well as deposits of Ig in their kidney glomeruli. Thus, NOD mice immunized with MIV-7 developed both autoantibodies and clinical features of SLE. The MIV-7-treated mice, however, showed a significantly lower incidence of IDDM (25{\%} vs. 90{\%}, P",
keywords = "Autoantibodies, Diabetes, Idiotypes, NOD, SLE",
author = "I. Krause and Yaron Tomer and D. Elias and M. Blank and B. Gilburd and Cohen, {I. R.} and Y. Shoenfeld",
year = "1999",
month = "8",
doi = "10.1006/jaut.1999.0292",
language = "English (US)",
volume = "13",
pages = "49--55",
journal = "Journal of Autoimmunity",
issn = "0896-8411",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - Inhibition of diabetes in NOD mice by idiotypic induction of SLE

AU - Krause, I.

AU - Tomer, Yaron

AU - Elias, D.

AU - Blank, M.

AU - Gilburd, B.

AU - Cohen, I. R.

AU - Shoenfeld, Y.

PY - 1999/8

Y1 - 1999/8

N2 - The present study was undertaken to investigate whether active induction of systemic lupus erythematosus (SLE) in non-obese diabetic (NOD) mice could affect their development of insulin-dependent diabetes mellitus (IDDM). NOD mice were immunized with a human IgM mAb carrying the 16/6 idiotype (MIV-7) or with control human IgM. The mice were bled monthly and tested for SLE- associated autoantibodies in the serum and for the presence of leukopenia, thrombocytopenia, proteinuria and immunoglobulin deposits in the kidneys. The development of diabetes was determined by a blood glucose level exceeding 15 mM on two consecutive weekly determinations and by the presence of insulitis in the pancreas. The NOD mice immunized with MIV-7 developed high and persistent levels of autoantibodies, including anti-DNA, anti-histones and anti-cardiolipin, untreated mice and those immunized with normal human IgM did not produce these autoantibodies. The MIV-7-immunized mice also manifested an elevated erythrocyte sedimentation rate, leukopenia, thrombocytopenia and significant proteinuria, as well as deposits of Ig in their kidney glomeruli. Thus, NOD mice immunized with MIV-7 developed both autoantibodies and clinical features of SLE. The MIV-7-treated mice, however, showed a significantly lower incidence of IDDM (25% vs. 90%, P

AB - The present study was undertaken to investigate whether active induction of systemic lupus erythematosus (SLE) in non-obese diabetic (NOD) mice could affect their development of insulin-dependent diabetes mellitus (IDDM). NOD mice were immunized with a human IgM mAb carrying the 16/6 idiotype (MIV-7) or with control human IgM. The mice were bled monthly and tested for SLE- associated autoantibodies in the serum and for the presence of leukopenia, thrombocytopenia, proteinuria and immunoglobulin deposits in the kidneys. The development of diabetes was determined by a blood glucose level exceeding 15 mM on two consecutive weekly determinations and by the presence of insulitis in the pancreas. The NOD mice immunized with MIV-7 developed high and persistent levels of autoantibodies, including anti-DNA, anti-histones and anti-cardiolipin, untreated mice and those immunized with normal human IgM did not produce these autoantibodies. The MIV-7-immunized mice also manifested an elevated erythrocyte sedimentation rate, leukopenia, thrombocytopenia and significant proteinuria, as well as deposits of Ig in their kidney glomeruli. Thus, NOD mice immunized with MIV-7 developed both autoantibodies and clinical features of SLE. The MIV-7-treated mice, however, showed a significantly lower incidence of IDDM (25% vs. 90%, P

KW - Autoantibodies

KW - Diabetes

KW - Idiotypes

KW - NOD

KW - SLE

UR - http://www.scopus.com/inward/record.url?scp=0032803292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032803292&partnerID=8YFLogxK

U2 - 10.1006/jaut.1999.0292

DO - 10.1006/jaut.1999.0292

M3 - Article

C2 - 10441167

AN - SCOPUS:0032803292

VL - 13

SP - 49

EP - 55

JO - Journal of Autoimmunity

JF - Journal of Autoimmunity

SN - 0896-8411

IS - 1

ER -