Contributions
Abstract: P974
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
A pro-inflammatory T cell population expressing the B cell marker CD20 has been described in the blood and the brain of patients with Multiple Sclerosis (MS). These cells are associated with a Th17-like phenotype and are sensitive to depletion by rituximab. However, there is still limited knowledge on their function or possible involvement with MS pathogenesis.
We investigated the phenotype of CD20+ T cells in the blood and CSF of MS and control patients using flow cytometry, and performed in vitro cell culture on highly purified sorted cells to assess proliferation and function.
We confirmed previous findings that CD20+ T cells co-express CD3 and CD20 at the protein and mRNA level, are found in all major T cell subsets and are over-represented in the CD8+ memory T cell compartment. We identified CD20+ T cells in the CSF of both MS and control patients at similar frequencies, where they expressed increased IFNy and CCR6, but not IL-17, in comparison to conventional CSF T cells. CD20+ T cells expressed elevated PD-1 and displayed diminished proliferative capacity compared to CD20- T cells, but retained potent cytolytic potential. Finally, CD20 was maintained in vitro under resting conditions and following stimulation, and was not inducible in culture following stimulation.
These findings demonstrate that CD20+ T cells display a stable effector phenotype, with expression of inhibitory receptors and reduced proliferation, consistent with a highly differentiated but functional state. These cells may enter the CSF where their pro-inflammatory properties are retained, and therefore have the potential to contribute to the pathogenesis of MS. It remains to be determined whether the CNS antigen-specific T cell population includes CD20+ T cells.
Disclosure: Nothing to disclose
Abstract: P974
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 15 Immunology
A pro-inflammatory T cell population expressing the B cell marker CD20 has been described in the blood and the brain of patients with Multiple Sclerosis (MS). These cells are associated with a Th17-like phenotype and are sensitive to depletion by rituximab. However, there is still limited knowledge on their function or possible involvement with MS pathogenesis.
We investigated the phenotype of CD20+ T cells in the blood and CSF of MS and control patients using flow cytometry, and performed in vitro cell culture on highly purified sorted cells to assess proliferation and function.
We confirmed previous findings that CD20+ T cells co-express CD3 and CD20 at the protein and mRNA level, are found in all major T cell subsets and are over-represented in the CD8+ memory T cell compartment. We identified CD20+ T cells in the CSF of both MS and control patients at similar frequencies, where they expressed increased IFNy and CCR6, but not IL-17, in comparison to conventional CSF T cells. CD20+ T cells expressed elevated PD-1 and displayed diminished proliferative capacity compared to CD20- T cells, but retained potent cytolytic potential. Finally, CD20 was maintained in vitro under resting conditions and following stimulation, and was not inducible in culture following stimulation.
These findings demonstrate that CD20+ T cells display a stable effector phenotype, with expression of inhibitory receptors and reduced proliferation, consistent with a highly differentiated but functional state. These cells may enter the CSF where their pro-inflammatory properties are retained, and therefore have the potential to contribute to the pathogenesis of MS. It remains to be determined whether the CNS antigen-specific T cell population includes CD20+ T cells.
Disclosure: Nothing to disclose