Immunoregulation

Brent, L.

doi:10.1016/b978-012131770-6/50026-2

Cited by 5 publications

(1 citation statement)

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“…The notion of tolerance became accepted during the 1960s and successive theoretical and practical contributions from several distinguished scientists eventually revealed the basic mechanisms involved and the substantial importance of their findings [ 2 , 3 ]. For example, Bretscher and Cohn [ 4 ] offered criteria to fulfil the theory of self-/non-self-discrimination and tolerance to auto-antigens while the practical significance of immunological tolerance was subsequently expounded by Brent [ 5 ] and referred to as ‘the holy grail of transplantation research.’…”

Section: Introductionmentioning

confidence: 99%

An evaluation of the recognised systemic inflammatory biomarkers of chronic sub-optimal inflammation provides evidence for inflammageing (IFA) during multiple sclerosis (MS)

Bolton¹

2021

Immun Ageing

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The pathogenesis of the human demyelinating disorder multiple sclerosis (MS) involves the loss of immune tolerance to self-neuroantigens. A deterioration in immune tolerance is linked to inherent immune ageing, or immunosenescence (ISC). Previous work by the author has confirmed the presence of ISC during MS. Moreover, evidence verified a prematurely aged immune system that may change the frequency and profile of MS through an altered decline in immune tolerance. Immune ageing is closely linked to a chronic systemic sub-optimal inflammation, termed inflammageing (IFA), which disrupts the efficiency of immune tolerance by varying the dynamics of ISC that includes accelerated changes to the immune system over time. Therefore, a shifting deterioration in immunological tolerance may evolve during MS through adversely-scheduled effects of IFA on ISC. However, there is, to date, no collective proof of ongoing IFA during MS. The Review addresses the constraint and provides a systematic critique of compelling evidence, through appraisal of IFA-related biomarker studies, to support the occurrence of a sub-optimal inflammation during MS. The findings justify further work to unequivocally demonstrate IFA in MS and provide additional insight into the complex pathology and developing epidemiology of the disease.

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