Cytotoxic CX3CR1+ T cells drive vascular inflammation in giant cell arteritis but not in Takayasu's arteritis.

Autor:	Inukai R; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Akiyama M; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan. mitsuaki@keio.jp., Yoshimoto K; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Wakasugi S; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Matsuno Y; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Ishigaki S; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Alshehri W; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Saito K; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan., Kaneko Y; Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Jazyk:	angličtina
Zdroj:	Clinical and experimental rheumatology [Clin Exp Rheumatol] 2024 Oct 21. Date of Electronic Publication: 2024 Oct 21.
DOI:	10.55563/clinexprheumatol/jmrl3k
Abstrakt:	Objectives: To compare the involvement of cytotoxic CX3CR1+ T cell subsets between giant cell arteritis (GCA) and Takayasu's arteritis (TAK). Methods: We examined the proportions of CX3CR1+ CD4+ and CD8+ T cells in whole blood freshly obtained from 30 treatment-naive patients with active large vessel vasculitis (GCA, n=22 and TAK, n=8) and 16 healthy controls (HC). Infiltration of CX3CR1+ T cells into the affected arteries was assessed using immunohistochemical staining. Furthermore, CX3CR1+ CD4+ and CD8+ T cells were followed up after glucocorticoid treatment for longitudinal assessment of both diseases. Results: The proportion of CX3CR1+ CD4+ T cells was significantly higher in GCA than in HC but not in TAK. No differences were observed in the proportions of CX3CR1+ CD8+ T cells among the GCA, TAK, and HC groups. The increased proportion of CX3CR1+ CD4+ T cells in GCA strongly correlated with the severity of systemic inflammation, whereas no significant correlation was found in TAK. Compared to TAK, CX3CR1+ CD4+ T cells from GCA patients showed significantly higher expression of granzyme B and perforin. The inflamed temporal arterial tissues of the GCA were infiltrated by numerous CX3CR1+ T cells, contributing to inflammation, disruption of the elastic lamina, and intimal hyperplasia. In contrast, no infiltration of CX3CR1+ T cells was observed in the aortitis lesions of TAK. Longitudinal analysis of post-glucocorticoid treatment showed a reduction in CX3CR1+ T cells in GCA, whereas no significant change was observed in TAK. Conclusions: Differences in immune mechanisms between GCA and TAK highlight cytotoxic CX3CR1+ T cells as potential drivers for GCA-related inflammation and vessel damage but not for TAK.
Databáze:	MEDLINE
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