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T-helper 2 regulatory cells (Th2(reg)) are a functional subset of CD4+ T-lymphocytes characterized by their ability to produce anti-inflammatory and neurotrophic factors [MDPI, 2024; PNAS, 2000]. Unlike proinflammatory Th2 cells that drive allergic responses, Th2(reg) cells suppress pathogenic Th1 and Th17 immune responses by secreting cytokines such as IL-4, IL-10, and TGF-beta [NIH, 2024; MDPI, 2020]. They are highly relevant in neurodegenerative and autoimmune conditions, where they contribute to neuroprotection through the secretion of factors like brain-derived neurotrophic factor (BDNF) [PNAS, 2000]. Therapeutic strategies, most notably the use of glatiramer acetate (Copaxone), aim to induce a shift in the T-cell population toward this regulatory phenotype to treat diseases like multiple sclerosis [MDPI, 2024; Lenus, 2024]. Dysregulation of these cells is also observed in Parkinson’s disease, where a lack of regulatory control contributes to neuroinflammation [MDPI, 2020; PMC, 2019]. Monitoring the levels of signature Th2 cytokines and transcription factors like GATA3 serves as a vital biomarker for assessing therapeutic efficacy and patient response [Creative Diagnostics, 2024].
Induction of anti-inflammatory T-cell differentiation; glatiramer acetate acts as a myelin basic protein (MBP) decoy by binding to MHC class II and the T-cell receptor (TCR), promoting an immune deviation from proinflammatory Th1 cells to anti-inflammatory Th2 regulatory cells [MDPI, 2024; Lenus, 2024].
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