We are analyzing https://link.springer.com/article/10.1186/s12979-020-00178-w.

Title:
Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression | Immunity & Ageing
Description:
Patients with rheumatoid arthritis (RA) develop features of accelerated ageing, including immunosenescence. These changes include decreased thymic functionality, expansion of late-differentiated effector T cells, increased telomeric attrition, and excessive production of cytokines (senescence-associated secretory phenotype). The progression of RA has been associated with the early development of age-related co-morbidities, including osteoporosis, cardiovascular complications, and cognitive impairment. Here I review data supporting the hypothesis that immune-senescence contributes to the aggravation of both articular and extra-articular manifestations. Of note, poor cognitive functions in RA were associated with senescent CD28- T cells, inflammaging, and autoantibodies against brain antigens. The pathways of immune-to-brain communication are discussed and provide the rationale for the cognitive impairment reported in RA.
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Keywords {🔍}

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Topics {✒️}

eomesodermin-expressing t-helper cells coenen-de roo cjj das28/c-reactive protein hla-dr β chain steroidal anti-inflammatory drugs brain-derived neurotrophic factor t-cell receptor diversity article download pdf anti-citrullinated protein antibody undergone post-translational modification integrating single-cell transcriptomics extra-chromosomal dna sequences n-methyl-d-aspartate bone marrow-derived microglia immune-modulated glutamatergic neurotransmission osteoclast-mediated bone resorption cytokine-induced depressive symptoms complete t-cell activation splenic t-cell subset central nervous system derived molecules cross-talk anti-tnf-α therapy [97] inflammatory reflex--linking immunity systemic low-grade inflammation immune-senescent profile observed inhibited tnf-α production cytotoxic virus-specific cd4+ van den berg recent meta-analysis explored c-reactive protein cholinergic anti-inflammatory pathway attenuating tnf-α levels stress-induced metabolic disorder lps-induced sickness behaviour peripheral pro-inflammatory cytokines age-matched healthy controls decreased food-motivated behaviour bmc musculoskelet disord solomon dh t-cell repertoire nuclease mre11a induces human herpes virus-6 key transcription factor anti-citrullinated antibodies decreased circulating cd28-negative privacy choices/manage cookies rheumatology biologics register extra-articular manifestations including cell-derived xanthine nuclear factor-κb

Questions {❓}

Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: A neuroprotective role of inflammation?
Aging of the immune system: A risk factor for autoimmunity?
Can early immunosenescence be detected in the preclinical phase of RA, or is it a consequence of established disease?
Has cytomegalovirus infection any role in the development of atherosclerosis?
Homocysteine and inflammation: predictors of cognitive decline in older persons?
How do immune cells support and shape the brain in health, disease, and aging?
How do pro-inflammatory cytokines promote depressive behaviour?
Immunosenescence and rheumatoid arthritis: does telomere shortening predict impending disease?
Inflammation in psychiatric disorders: what comes first?
Interleukin-1beta in immune cells of the abdominal vagus nerve: a link between the immune and nervous systems?
Is there any evidence that neurotrophins are altered in RA?
Severe depression is associated with increased microglial quinolinic acid in subregions of the anterior cingulate gyrus: evidence for an immune-modulated glutamatergic neurotransmission?
The story of CD4+CD28- T cells revisited: solved or still ongoing?

Schema {🗺️}

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         headline:Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression
         description:Patients with rheumatoid arthritis (RA) develop features of accelerated ageing, including immunosenescence. These changes include decreased thymic functionality, expansion of late-differentiated effector T cells, increased telomeric attrition, and excessive production of cytokines (senescence-associated secretory phenotype). The progression of RA has been associated with the early development of age-related co-morbidities, including osteoporosis, cardiovascular complications, and cognitive impairment. Here I review data supporting the hypothesis that immune-senescence contributes to the aggravation of both articular and extra-articular manifestations. Of note, poor cognitive functions in RA were associated with senescent CD28- T cells, inflammaging, and autoantibodies against brain antigens. The pathways of immune-to-brain communication are discussed and provide the rationale for the cognitive impairment reported in RA.
         datePublished:2020-03-09T00:00:00Z
         dateModified:2020-03-09T00:00:00Z
         pageStart:1
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            Ageing
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            Immune ageing
            Cognitive impairment
            Immunology
            Geriatrics/Gerontology
            Aging
            Public Health
            Clinical Nutrition
            Antibodies
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ScholarlyArticle:
      headline:Accelerated immunosenescence in rheumatoid arthritis: impact on clinical progression
      description:Patients with rheumatoid arthritis (RA) develop features of accelerated ageing, including immunosenescence. These changes include decreased thymic functionality, expansion of late-differentiated effector T cells, increased telomeric attrition, and excessive production of cytokines (senescence-associated secretory phenotype). The progression of RA has been associated with the early development of age-related co-morbidities, including osteoporosis, cardiovascular complications, and cognitive impairment. Here I review data supporting the hypothesis that immune-senescence contributes to the aggravation of both articular and extra-articular manifestations. Of note, poor cognitive functions in RA were associated with senescent CD28- T cells, inflammaging, and autoantibodies against brain antigens. The pathways of immune-to-brain communication are discussed and provide the rationale for the cognitive impairment reported in RA.
      datePublished:2020-03-09T00:00:00Z
      dateModified:2020-03-09T00:00:00Z
      pageStart:1
      pageEnd:14
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12979-020-00178-w
      keywords:
         Rheumatoid arthritis
         Ageing
         Cell senescence
         Immune ageing
         Cognitive impairment
         Immunology
         Geriatrics/Gerontology
         Aging
         Public Health
         Clinical Nutrition
         Antibodies
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      name:School of Health and Life Sciences, Pontifical Catholic University of Rio Grande do Sul (PUCRS)
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      name:Laboratory of Immunobiology, School of Health and Life Sciences, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre, Brazil

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