âMultiple sclerosis (MS) is the most common autoimmune demyelinating disease in human and T helper type 2 (Th2) cells have been shown to be beneficial for this disease. However, mechanisms by which Th2 cells ameliorate disease in MS are poorly understood. Microglial activation plays an important role in the pathogenesis of MS and other neurodegenerative disorders. Here, we delineate that Th2 cells are capable of suppressing microglial activation via cell-to-cell contact. After polarization of MBP-primed Th1 cells to Th2 by gemfibrozil and other drugs, we observed that MBP-primed Th2 cells dose dependently inhibited the production of interleukin-1Î² (IL-1Î²) and nitric oxide (NO) in LPS-stimulated microglia via cell-to-cell contact. Similarly, Th2 cells also suppressed the microglial inflammatory response in the presence of different pathological stimuli of Alzheimerâs disease (AD), Parkinsonâs disease (PD), and HIV associated dementia (HAD). Interestingly, Th2 cells expressed higher levels of alphaV (Î±V) and beta3 (Î²3) integrins as compared to Th1 cells, and functional blocking antibodies against Î±V and Î²3 integrins impaired the ability of Th2 cells to suppress microglial activation. Furthermore, we demonstrate that microglia expressed the beta subunit of PDGF receptor (PDGFRÎ²) and that neutralization of PDGFRÎ² abrogated the ability of Th2 cells to suppress microglial inflammationâ Roy A, et al. Myelin Basic Protein-primed T Helper 2 Cells Suppress Microglial Activation via AlphaVBeta3 Integrin: Implications for Multiple Sclerosis.
Journal of Multiple Sclerosis provides information on recent studies in multiple sclerosis.
Last date updated on June, 2014