SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice

Howard Dang, Andrew G. Geiser, John J. Letterio, Toru Nakabayashi, Liping Kong, Gabriel Fernandes, Norman Talal

Research output: Contribution to journalArticle

154 Citations (Scopus)

Abstract

Original languageEnglish
Pages (from-to)3205-3212
Number of pages8
JournalJournal of Immunology
Volume155
Issue number6
StatePublished - 1995

Fingerprint

Knockout Mice
Autoantibodies
Pseudolymphoma
Ribonucleoproteins
Rheumatoid Factor
Serology
Immunosuppressive Agents
Heterozygote
Salivary Glands
Serum
Dexamethasone
Autoimmune Diseases
Immunoglobulin M
Immunoglobulin G
Western Blotting
Enzyme-Linked Immunosorbent Assay
Cytokines
Lung
Mutation

ASJC Scopus subject areas

  • Immunology

Cite this

Dang, H., Geiser, A. G., Letterio, J. J., Nakabayashi, T., Kong, L., Fernandes, G., & Talal, N. (1995). SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice. Journal of Immunology, 155(6), 3205-3212.

SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice. / Dang, Howard; Geiser, Andrew G.; Letterio, John J.; Nakabayashi, Toru; Kong, Liping; Fernandes, Gabriel; Talal, Norman.

In: Journal of Immunology, Vol. 155, No. 6, 1995, p. 3205-3212.

Research output: Contribution to journalArticle

Dang, H, Geiser, AG, Letterio, JJ, Nakabayashi, T, Kong, L, Fernandes, G & Talal, N 1995, 'SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice', Journal of Immunology, vol. 155, no. 6, pp. 3205-3212.
Dang H, Geiser AG, Letterio JJ, Nakabayashi T, Kong L, Fernandes G et al. SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice. Journal of Immunology. 1995;155(6):3205-3212.
Dang, Howard ; Geiser, Andrew G. ; Letterio, John J. ; Nakabayashi, Toru ; Kong, Liping ; Fernandes, Gabriel ; Talal, Norman. / SLE-like autoantibodies and Sjögren's syndrome-like lymphoproliferation in TGF-ß knockout mice. In: Journal of Immunology. 1995 ; Vol. 155, No. 6. pp. 3205-3212.
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title = "SLE-like autoantibodies and Sj{\"o}gren's syndrome-like lymphoproliferation in TGF-{\ss} knockout mice",
abstract = "Mice bearing the TGF-β1 null mutation (-/-) develop lymphoid infiltrates in the heart, lungs, salivary glands, and other organs similar to those seen in the pseudolymphoma of Sj{\"o}gren's Syndrome. We studied sera from -/- mice and found elevated Ab levels to dsDNA, ssDNA, and Sm ribonucleoprotein. No Abs to SSA/Ro or SSB/La and no IgM rheumatoid factor were found. Serum autoantibodies were predominately IgG and were specific as shown by ELISA inhibition studies. Antinuclear Ab patterns on Western blots varied from one mouse to the next, indicating a random process responsible for the diversity. Wild-type and heterozygote mice had no autoantibodies. Ig glomerular deposits were found in -/- mice, indicating that these autoantibodies may be pathogenic. Treatment of -/- mice with dexamethasone or TGF-β1 failed to suppress autoantibody production. These mice represent an overlap combining the autoimmune serology of SLE with the tissue infiltrates of SS. Our results support the concept that TGF-β1 is an important naturally occurring immunosuppressive cytokine whose absence can lead to a sys-temic autoimmune disease.",
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AU - Dang, Howard

AU - Geiser, Andrew G.

AU - Letterio, John J.

AU - Nakabayashi, Toru

AU - Kong, Liping

AU - Fernandes, Gabriel

AU - Talal, Norman

PY - 1995

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N2 - Mice bearing the TGF-β1 null mutation (-/-) develop lymphoid infiltrates in the heart, lungs, salivary glands, and other organs similar to those seen in the pseudolymphoma of Sjögren's Syndrome. We studied sera from -/- mice and found elevated Ab levels to dsDNA, ssDNA, and Sm ribonucleoprotein. No Abs to SSA/Ro or SSB/La and no IgM rheumatoid factor were found. Serum autoantibodies were predominately IgG and were specific as shown by ELISA inhibition studies. Antinuclear Ab patterns on Western blots varied from one mouse to the next, indicating a random process responsible for the diversity. Wild-type and heterozygote mice had no autoantibodies. Ig glomerular deposits were found in -/- mice, indicating that these autoantibodies may be pathogenic. Treatment of -/- mice with dexamethasone or TGF-β1 failed to suppress autoantibody production. These mice represent an overlap combining the autoimmune serology of SLE with the tissue infiltrates of SS. Our results support the concept that TGF-β1 is an important naturally occurring immunosuppressive cytokine whose absence can lead to a sys-temic autoimmune disease.

AB - Mice bearing the TGF-β1 null mutation (-/-) develop lymphoid infiltrates in the heart, lungs, salivary glands, and other organs similar to those seen in the pseudolymphoma of Sjögren's Syndrome. We studied sera from -/- mice and found elevated Ab levels to dsDNA, ssDNA, and Sm ribonucleoprotein. No Abs to SSA/Ro or SSB/La and no IgM rheumatoid factor were found. Serum autoantibodies were predominately IgG and were specific as shown by ELISA inhibition studies. Antinuclear Ab patterns on Western blots varied from one mouse to the next, indicating a random process responsible for the diversity. Wild-type and heterozygote mice had no autoantibodies. Ig glomerular deposits were found in -/- mice, indicating that these autoantibodies may be pathogenic. Treatment of -/- mice with dexamethasone or TGF-β1 failed to suppress autoantibody production. These mice represent an overlap combining the autoimmune serology of SLE with the tissue infiltrates of SS. Our results support the concept that TGF-β1 is an important naturally occurring immunosuppressive cytokine whose absence can lead to a sys-temic autoimmune disease.

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