NDLI: The mechanism by which a peptide based on complementarity-determining region-1 of a pathogenic anti-DNA auto-Ab ameliorates experimental systemic lupus erythematosus.

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The mechanism by which a peptide based on complementarity-determining region-1 of a pathogenic anti-DNA auto-Ab ameliorates experimental systemic lupus erythematosus.

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The mechanism by which a peptide based on complementarity-determining region-1 of a pathogenic anti-DNA auto-Ab ameliorates experimental systemic lupus erythematosus.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mozes, E. Eilat, E. Dayan, M. Zinger, H.
Description	Author Affiliation: Eilat E ( Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel.);
Abstract	A peptide based on complementarity-determining region (CDR)-1 of a monoclonal murine anti-DNA Ab that bears the common idiotype, 16/6Id, was synthesized and characterized. The peptide, designated pCDR1, was found to be an immunodominant T-cell epitope in BALB/c mice. The CDR1-based peptide was shown to be capable of inhibiting the in vivo priming of BALB/c mice immunized with the peptide or with the whole anti-DNA 16/6Id(+) mAbs of either mouse or human origin. We show here that administration of pCDR1 (weekly, i.v., 100 microgram/mouse) in aqueous solution for 5 weeks starting at the time of disease induction with the human 16/6Id prevented the development of clinical manifestations of experimental systemic lupus erythematosus (SLE). Further, 10 weekly injections of pCDR1 to BALB/c mice with an established experimental SLE down-regulated clinical manifestations of SLE (e.g., anti-DNA auto-Abs, leukopenia, proteinuria, immune complex deposits in the kidneys) in the treated mice. Prevention of SLE induction was shown to be associated mainly with a decrease in the levels of IL-2, INFgamma, and the proinflammatory cytokine TNFalpha. On the other hand, the secretion of the immunosuppressive cytokine TGFbeta was elevated. Amelioration of the clinical manifestations of an already established experimental SLE correlated with a dramatic decrease in TNFalpha secretion, elevated levels of TGFbeta, and immunomodulation of the Th1 and Th2 type cytokines to levels close to those observed in healthy mice.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	3
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antibodies, Antinuclear Immunology Antibodies, Monoclonal Immunoglobulin Fragments Therapeutic Use Lupus Erythematosus, Systemic Prevention & Control Amino Acid Sequence Animals Blood Chemistry Cells, Cultured Cytokines Biosynthesis Disease Models, Animal Drug Administration Schedule Enzyme-Linked Immunosorbent Assay Epitopes Administration & Dosage Injections, Intravenous Injections, Subcutaneous Pathology Lymphocytes Mice Mice, Inbred BALB C Molecular Sequence Data Spleen T-Lymphocytes Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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