CD4+ T Cells as Key Players in the Immunopathology of Takayasu Arteritis: Comment on the Article by

Watanabe, Ryu

doi:10.1002/art.41198

Cited by 2 publications

(2 citation statements)

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“…Taken together, these results indicate that GCA and TAK have critical differences in immune cell composition in the peripheral blood and within the vasculitic lesions. CD4 + T cells and CD8 + T cells in TAK patients share sustained mTORC1 activity (14,154,155). Upstream signals that drive activation of the mTORC1 pathway have not yet been defined and our understanding of the functional consequences for protective and pathogenic immunity in these patients is limited.…”

Section: Cd8 + T Cellsmentioning

confidence: 99%

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Cellular Signaling Pathways in Medium and Large Vessel Vasculitis

et al. 2020

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Autoimmune and autoinflammatory diseases of the medium and large arteries, including the aorta, cause life-threatening complications due to vessel wall destruction but also by wall remodeling, such as the formation of wall-penetrating microvessels and lumenstenosing neointima. The two most frequent large vessel vasculitides, giant cell arteritis (GCA) and Takayasu arteritis (TAK), are HLA-associated diseases, strongly suggestive for a critical role of T cells and antigen recognition in disease pathogenesis. Recent studies have revealed a growing spectrum of effector functions through which T cells participate in the immunopathology of GCA and TAK; causing the disease-specific patterning of pathology and clinical outcome. Core pathogenic features of disease-relevant T cells rely on the interaction with endothelial cells, dendritic cells and macrophages and lead to vessel wall invasion, formation of tissue-damaging granulomatous infiltrates and induction of the name-giving multinucleated giant cells. Besides antigen, pathogenic T cells encounter danger signals in their immediate microenvironment that they translate into disease-relevant effector functions. Decisive signaling pathways, such as the AKT pathway, the NOTCH pathway, and the JAK/STAT pathway modify antigen-induced T cell activation and emerge as promising therapeutic targets to halt disease progression and, eventually, reset the immune system to reestablish the immune privilege of the arterial wall.

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Section: Cd8 + T Cellsmentioning

confidence: 99%

“…CD4 + T cells and CD8 + T cells in TAK patients share sustained mTORC1 activity ( 14 , 154 , 155 ). Upstream signals that drive activation of the mTORC1 pathway have not yet been defined and our understanding of the functional consequences for protective and pathogenic immunity in these patients is limited.…”

Section: Takayasu’s Arteritismentioning

confidence: 99%