Interleukin 37; a possible marker of arterial stiffness in Behçet's disease

Hussein, Mohamed; Ramadan, Mostafa; Moneam, Manal Abd El; Halim, Hanan Abd El; Ghaffar, Nagwa Abd El; Fawzy, Mary

doi:10.1016/j.amjms.2022.04.013

Cited by 4 publications

(1 citation statement)

References 37 publications

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“…IL37, a member of the IL1 family, exerts an anti-inflammatory activity (121). It has been linked to various diseases like SLE (122), arterial stiffness in Behcet's disease (123), and inflammatory osteoarticular diseases (124). IL37 has been shown to inhibit innate immunity (125) but more recently, Cavalli et al demonstrated that IL37 can block trained immunity changes.…”

Section: Discussionmentioning

confidence: 99%

Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology

Beignon

Galeotti²,

Schvartz³

2023

Front. Med.

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Autoimmune disorders have been well characterized over the years and many pathways—but not all of them–have been found to explain their pathophysiology. Autoinflammatory disorders, on the other hand, are still hiding most of their molecular and cellular mechanisms. During the past few years, a newcomer has challenged the idea that only adaptive immunity could display memory response. Trained immunity is defined by innate immune responses that are faster and stronger to a second stimulus than to the first one, being the same or not. In response to the trained immunity inducer, and through metabolic and epigenetic changes of hematopoietic stem and progenitor cells in the bone marrow that are transmitted to their cellular progeny (peripheral trained immunity), or directly of tissue-resident cells (local innate immunity), innate cells responsiveness and functions upon stimulation are improved in the long-term. Innate immunity can be beneficial, but it could also be detrimental when maladaptive. Here, we discuss how trained immunity could contribute to the physiopathology of autoimmune and autoinflammatory diseases.

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