ArticleArthritis research & therapy2012
Local delivery of AAV2-CTLA4IgG decreases sialadenitis and improves gland function in the C57BL/6.NOD-Aec1Aec2 mouse model of Sjögren's syndrome.
Article in Arthritis research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- The role and function of CTLA-4 in Sjögren's syndrome.Frontiers in immunology · 2026Review
- Exploring MHC class II I-Ab blockade as a potential treatment for Sjögren's disease in the mouse model.ImmunoHorizons · 2025Article
- Review
- Correction of LAMP3-associated salivary gland hypofunction by aquaporin gene therapy.Scientific reports · 2022Article
- Stimulation of regulatory T cells with Lactococcus lactis expressing enterotoxigenic E. coli colonization factor antigen 1 retains salivary flow in a genetic model of Sjögren's syndrome.Arthritis research & therapy · 2021Article
- Transduction of Salivary Gland Acinar Cells with a Novel AAV Vector 44.9.Molecular therapy. Methods & clinical development · 2020Article
- Rheumatic Manifestations in Patients Treated with Immune Checkpoint Inhibitors.International journal of molecular sciences · 2020Review
- Inhibition of lysophosphatidic acid receptor ameliorates Sjögren's syndrome in NOD mice.Oncotarget · 2017Article
- Neutralizing antibodies against adeno-associated viruses in Sjögren's patients: implications for gene therapy.Gene therapy · 2017Article
- Smad4 in T cells plays a protective role in the development of autoimmune Sjögren's syndrome in the nonobese diabetic mouse.Oncotarget · 2016Article
- Dysregulated co-stimulatory molecule expression in a Sjögren's syndrome mouse model with potential implications by microRNA-146a.Molecular immunology · 2015Article
- IL-17 sequestration via salivary gland gene therapy in a mouse model of Sjogren's syndrome suppresses disease-associated expression of the putative autoantigen Klk1b22.Arthritis research & therapy · 2015Article
- The clinical relevance of animal models in Sjögren's syndrome: the interferon signature from mouse to man.Arthritis research & therapy · 2015Review
- Observational
- Advances in salivary gland gene therapy - oral and systemic implications.Expert opinion on biological therapy · 2015Review
- Mouse Models of Primary Sjogren's Syndrome.Current pharmaceutical design · 2015Review
- Immune checkpoint receptors in regulating immune reactivity in rheumatic disease.Arthritis research & therapy · 2014Review
- Article
- Association of bone morphogenetic protein 6 with exocrine gland dysfunction in patients with Sjögren's syndrome and in mice.Arthritis and rheumatism · 2013Article
- Childhood Sjögren syndrome: insights from adults and animal models.Current opinion in rheumatology · 2013Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionCytotoxic T-lymphocyte antigen 4 (CTLA-4) is a key negative costimulatory molecule that displays a wide range of anti-inflammatory properties and is currently approved to treat rheumatoid arthritis as a recombinant fusion protein (CTLA4IgG). To better understand the role of CTLA4IgG in primary Sjögren's syndrome (pSS), we generated a recombinant adeno-associated virus vector serotype 2 (AAV2) expressing a chimera of mouse CTLA-4 fused with a human immunoglobulin (AAV2-CTLA4IgG) and observed the effect of this molecule in C57BL/6.NOD-Aec1Aec2 mice, an animal model of pSS.
methodsA recombinant adeno-associated virus-2 (AAV-2) vector was constructed encoding a CTLA4IgG fusion protein. The AAV2-CTLA4IgG vector and an AAV2 control vector encoding beta galactosidase (LacZ) were administered by retrograde cannulation of the submandibular glands of C57BL/6.NOD-Aec1Aec2 mice. Protein expression was measured by ELISA and salivary glands were assessed for inflammation and activity.
resultsRecombinant CTLA4IgG blocked B7 expression on macrophages in vitro. In vivo, localized expression of CTLA4IgG in the salivary glands of C57BL/6.NOD-Aec1Aec2 mice inhibited the loss of salivary gland activity and decreased T and B cell infiltration as well as dendritic cells and macrophages in the glands compared with control mice. In addition a decrease in several proinflammatory cytokines and an increase in transforming growth factor beta-1 (TGF-β1) expression were also observed.
conclusionsThese data suggest expression of CTLA4IgG in the salivary gland can decrease the inflammation and improve the xerostomia reported in these mice.
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