Age-related immunosenescence in Behçet’s disease

Korkmaz, Cengiz

doi:10.1007/s00296-022-05144-x

Rheumatol Int

2022

DOI: 10.1007/s00296-022-05144-x

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Age-related immunosenescence in Behçet’s disease

Cengiz Korkmaz

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Cited by 2 publications

References 60 publications

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Shelterin dysfunction promotes CD4+ T cell senescence in Behçet’s disease

Shi,

Zhang,

Zhang

et al. 2023

Rheumatology

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Objectives To investigate the potential role of shelterin dysfunction in naïve CD4+ T cells in the pathogenesis of Behçet's disease (BD). Methods Naïve CD4+ T cells were isolated from 40 BD patients and 40 sex- and age-matched healthy controls (HC). Senescent profiles, shelterin subunits expression, telomere length, telomerase activity, and critical DNA damage response (DDR) was evaluated. TRF2 silencing was conducted for further validation. Results Compared to HC, BD patients had significantly decreased naïve CD4+ T cells, increased cell apoptosis, senescence, and productions of TNF-α and IFN-γ upon activation. Notably, BD naïve CD4+ T cells had shortened telomere, impaired telomerase activity, and expressed lower levels of shelterin subunits TRF2, TIN2, and RAP1. Furthermore, BD naïve CD4+ T cells exhibited significantly increased DDR, evidenced by elevated phosphorylated ataxia telangiectasia (AT) mutated (pATM), pp53, and p21. Finally, TRF2-silencing markedly upregulated DDR, apoptosis, and proinflammatory cytokines production in HC naïve CD4+ T cells. Conclusion Our study demonstrated that TRF2 deficiency in BD naïve CD4+ T cells promoted cell apoptosis and senescence, leading to proinflammatory cytokines overproduction. Therefore, restoring TRF2 might be a promising therapeutic strategy for BD.

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Shelterin dysfunction promotes CD4+ T cell senescence in Behçet’s disease

Shi,

Zhang,

Zhang

et al. 2023

Rheumatology

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Adamantiades‐Behcet's disease: From the first known descriptions to the era of the biologic agents

Stefanadi,

Dimitrakakis,

Dimitrakaki

et al. 2024

Int J of Rheum Dis

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In 1937, Dermatologist Hulusi Behcet presented a case of a patient with a 7-year history of recurrent ocular lesions, oral aphthous ulcers, and genital ulcers. The case report with the addition of a similar one was published in 1937. 1 Behcet published three more relevant papers most importantly pointing toward a single disease-syndrome from 1938 to 1940. In 1930, the Ophthalmologist Benedictos Adamantiades had described a case report of a disease with the title "A case of relapsing iritis with hypopyon." 2 Interestingly, we find Adamantiades-Behcet's disease (ABD) descriptions not only from Hippocrates of Kos but also from clinical observations similar to ABD disease recorded from 1772 to 1940. 3,4 Adamantiades-Behcet's disease (ABD) is a chronic, multisystem inflammatory disorder, which is clinically characterized mainly by relapsing oral aphthous, genital ulcers, ocular, and vascular lesions.The disease may affect small and large vessels in almost all organs. B-cell inhibitorsRituximab for ocular involvement Interleukin inhibitors monoclonal antibodiesAnakinra (IL 1) Canakinumab (IL1) Mucocutaneous involvement Ustekinumab (IL 12, IL 23) Tocilizumab (IL 6) Selective costimulation modulators Abatacept ocular, cutaneous involvement Apremilast phosphodiesterase inhibitor PDE4 Anti TNF Adalimumab, Infiximab eye, deep vein thrombosis, GI involvement, nervous system involvement Etanercept arthritis, mucocutaneous involvement TA B L E 2 Categories of biologic agents under study and in use.

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Age-related immunosenescence in Behçet’s disease

Cited by 2 publications

References 60 publications

Shelterin dysfunction promotes CD4+ T cell senescence in Behçet’s disease

Shelterin dysfunction promotes CD4+ T cell senescence in Behçet’s disease

Adamantiades‐Behcet's disease: From the first known descriptions to the era of the biologic agents

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