Contributions
Abstract: EP1480
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
Background: IL-24 is a cytokine of the IL-10 family and IL-20 subfamily. It shares receptor chains with IL-22 and IL-26, two cytokines which have shown to be associated with the IL-17 producing T helper (TH) subset TH17. It is well established that TH17 lymphocytes, as well as the cytokines they produce, are crucial in the pathogenesis of multiple sclerosis (MS). IL-24 has been shown to be elevated in patients with chronic inflammatory/autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease and psoriasis, however studies in MS are lacking. Here, we evaluate the unexplored role of IL-24 in MS.
Methods and results: Using quantitative PCR (qPCR), we show that IL-24 mRNA is expressed by activated T cells, B cells and monocytes of healthy donors (HD). In naive T cells, IL-24 mRNA is specifically induced by the combination of IL-6 and TGF-beta. Memory T cells, after differentiation into either TH1 or TH17 cells, express both IL-24 mRNA and protein, as assessed by qPCR and ELISA respectively, in HD and MS patients. Interestingly, the concentration of IL-24 is significantly higher in plasma samples of MS patients, compared to HD, as measured by ELISA. In our study cohort, immunomodulatory treatment significantly reduced the concentration of IL-24 in plasma samples. Using immunohistofluorescence on active MS lesions, we identified IL-24 expressing myelin-phagocytosing myeloid cells, as well as reactive astrocytes, which were both validated using in vitro cultures of primary human macrophages and astrocytes.
Conclusions: In summary, IL-24 is increased in the blood of MS patients, and it is expressed by activated lymphocytes, myelin-phagocytosing myeloid cells and reactive astrocytes in the context of neuroinflammation, warranting further investigation into its biological role in the context of MS.
Disclosure:
Bieke Broux: nothing to disclose in relation to this project.
Christian Peter: nothing to disclose in relation to this project.
Evelien Houben: nothing to disclose in relation to this project.
Lyne Bourbonnière: nothing to disclose in relation to this project.
Pierre Duquette: nothing to disclose in relation to this project.
Bart Van Wijmeersch: nothing to disclose in relation to this project.
Alexandre Prat: nothing to disclose in relation to this project.
Thomas Korn: nothing to disclose in relation to this project.
Niels Hellings: nothing to disclose in relation to this project.
Abstract: EP1480
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
Background: IL-24 is a cytokine of the IL-10 family and IL-20 subfamily. It shares receptor chains with IL-22 and IL-26, two cytokines which have shown to be associated with the IL-17 producing T helper (TH) subset TH17. It is well established that TH17 lymphocytes, as well as the cytokines they produce, are crucial in the pathogenesis of multiple sclerosis (MS). IL-24 has been shown to be elevated in patients with chronic inflammatory/autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease and psoriasis, however studies in MS are lacking. Here, we evaluate the unexplored role of IL-24 in MS.
Methods and results: Using quantitative PCR (qPCR), we show that IL-24 mRNA is expressed by activated T cells, B cells and monocytes of healthy donors (HD). In naive T cells, IL-24 mRNA is specifically induced by the combination of IL-6 and TGF-beta. Memory T cells, after differentiation into either TH1 or TH17 cells, express both IL-24 mRNA and protein, as assessed by qPCR and ELISA respectively, in HD and MS patients. Interestingly, the concentration of IL-24 is significantly higher in plasma samples of MS patients, compared to HD, as measured by ELISA. In our study cohort, immunomodulatory treatment significantly reduced the concentration of IL-24 in plasma samples. Using immunohistofluorescence on active MS lesions, we identified IL-24 expressing myelin-phagocytosing myeloid cells, as well as reactive astrocytes, which were both validated using in vitro cultures of primary human macrophages and astrocytes.
Conclusions: In summary, IL-24 is increased in the blood of MS patients, and it is expressed by activated lymphocytes, myelin-phagocytosing myeloid cells and reactive astrocytes in the context of neuroinflammation, warranting further investigation into its biological role in the context of MS.
Disclosure:
Bieke Broux: nothing to disclose in relation to this project.
Christian Peter: nothing to disclose in relation to this project.
Evelien Houben: nothing to disclose in relation to this project.
Lyne Bourbonnière: nothing to disclose in relation to this project.
Pierre Duquette: nothing to disclose in relation to this project.
Bart Van Wijmeersch: nothing to disclose in relation to this project.
Alexandre Prat: nothing to disclose in relation to this project.
Thomas Korn: nothing to disclose in relation to this project.
Niels Hellings: nothing to disclose in relation to this project.