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Start Over Author "Joly AL" Journal journal of autoimmunity
2 results on '"Joly AL"'

1. Multi-faceted inhibition of dendritic cell function by CD4 + Foxp3 + regulatory T cells.

Author

Seitz C, Liu S, Klocke K, Joly AL, Czarnewski PV, Tibbitt CA, Parigi SM, Westerberg LS, Coquet JM, Villablanca EJ, Wing K, and Andersson J

Subjects
Animals, CD4 Antigens metabolism, CTLA-4 Antigen genetics, Cell Differentiation, Cells, Cultured, Forkhead Transcription Factors genetics, Forkhead Transcription Factors metabolism, Gene Expression Profiling, Lymphocyte Activation, Lymphoproliferative Disorders genetics, Mice, Mice, Inbred C57BL, Mice, Transgenic, Pneumonia genetics, Programmed Cell Death 1 Ligand 2 Protein genetics, Programmed Cell Death 1 Ligand 2 Protein metabolism, Protein Isoforms genetics, CTLA-4 Antigen metabolism, Dendritic Cells immunology, Lymphoproliferative Disorders immunology, Pneumonia immunology, T-Lymphocytes, Regulatory immunology
Abstract

CTLA-4 is required for CD4 + Foxp3 + regulatory T (Treg) cell function, but its mode of action remains incompletely defined. Herein we generated Ctla-4 ex2fl/fl Foxp3-Cre mice with Treg cells exclusively expressing a naturally occurring, ligand-independent isoform of CTLA-4 (liCTLA-4) that cannot interact with the costimulatory molecules CD80 and CD86. The mice did not exhibit any signs of effector T cell activation early in life, however, at 6 months of age they exhibited excessive T cell activation and inflammation in lungs. In contrast, mice with Treg cells completely lacking CTLA-4 developed lymphoproliferative disease characterized by multi-organ inflammation early in life. In vitro, Treg cells exclusively expressing liCTLA-4 inhibited CD80 and CD86 expression on dendritic cells (DC). Conversely, Treg cells required the extra-cellular part of CTLA-4 to up-regulate expression of the co-inhibitory molecule PD-L2 on DCs. Transcriptomic analysis of suppressed DCs revealed that Treg cells induced a specific immunosuppressive program in DCs., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Published
2019
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2. Foxp3 lacking exons 2 and 7 is unable to confer suppressive ability to regulatory T cells in vivo.

Author

Joly AL, Liu S, Dahlberg CI, Mailer RK, Westerberg LS, and Andersson J

Subjects
Animals, Exons, Humans, Lymphocyte Activation genetics, Mice, Mice, Transgenic, Protein Isoforms genetics, Protein Isoforms immunology, T-Lymphocytes, Regulatory immunology, Forkhead Transcription Factors genetics, Forkhead Transcription Factors immunology, Forkhead Transcription Factors metabolism, T-Lymphocytes, Regulatory metabolism
Abstract

The forkhead/winged-helix transcription factor FOXP3 confers suppressive ability to CD4(+)FOXP3(+) regulatory T (Treg) cells. Human Treg cells express several different isoforms of FOXP3 that differ in function. However, the regulation and functional consequences of FOXP3 isoform expression remains poorly understood. In order to study the function of the FOXP3Δ2Δ7 isoform in vivo we generated mice that exclusively expressed a Foxp3 isoform lacking exon 2 and 7. These mice exhibited multi-organ inflammation, increased cytokine production, global T cell activation, activation of antigen-presenting cells and B cell developmental defects, all features that are shared with mice completely deficient in FOXP3. Our results demonstrate that the mouse counterpart of human FOXP3Δ2Δ7 is unable to confer suppressive ability to Treg cells., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Published
2015
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