Cytokine signatures in hereditary fever syndromes (HFS)
Highlights • The current review reports a number of advances in the field of inflammatory/immunological mechanisms underlying HFS, and presents all available data regarding the cytokines’ signatures in HFS at the transcriptional, serum and ex vivo levels. • It also integrates recent data in an updat...
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Published in | Cytokine & growth factor reviews Vol. 33; pp. 19 - 34 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Elsevier Ltd
01.02.2017
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Abstract | Highlights • The current review reports a number of advances in the field of inflammatory/immunological mechanisms underlying HFS, and presents all available data regarding the cytokines’ signatures in HFS at the transcriptional, serum and ex vivo levels. • It also integrates recent data in an updated classification of the different HFS in which CAPS, NLRP12AD and FMF were now classified as inflammasomopathies, HIDS/MKD as metabolic dysregulation leading to IL-1β secretion, and TRAPS and the last HFS identified to date, TRAPS11, as protein misfolding disorders. • Cytokine signatures obtained in patients’ cells cultured ex vivo are much more convincing than results obtained at the transcriptional levels or in sera. • Elevated levels of acute phase reactants and pro-inflammatory cytokines in remission periods confirm the involvement of the cytokine network in the inflammatory process and provide evidence for the ongoing subclinical inflammation during asymptomatic periods of HFS. • The marked increase of IL-1β production by LPS-stimulated PBMCs observed in CAPS and NLRP12AD, but also in FMF and MKD, is a hallmark of these disorders. |
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AbstractList | •The current review presents all available data regarding the cytokines’ signatures in HFS at the transcriptional, serum and ex vivo levels.•It also integrates recent data in an updated classification of the different HFS: CAPS, NLRP12AD, FMF, HIDS/MKD, TRAPS and TRAPS11.•Cytokine signatures in patients’ cells cultured ex vivo are much more convincing than results obtained at the transcriptional levels or in sera.•Pro-inflammatory cytokines are involved in the inflammatory process of HFS, even during remission periods.•The marked increase of IL-1β production by LPS-stimulated PBMCs observed in CAPS, NLRP12AD, FMF and MKD, is a hallmark of these disorders.
Hereditary fever syndromes (HFS) include a group of disorders characterized by recurrent self-limited episodes of fever accompanied by inflammatory manifestations occurring in the absence of infection or autoimmune reaction. Advances in the genetics of HFS have led to the identification of new gene families and pathways involved in the regulation of inflammation and innate immunity. The key role of several cytokine networks in the pathogenesis of HFS has been underlined by several groups, and supported by the rapid response of patients to targeted cytokine blocking therapies. This can be due to the direct effect of cytokine overproduction or to an absence of receptor antagonist resulting in dysbalance of downstream pro- and anti-inflammatory cytokine networks.
The aim of this study was to present an overview and to discuss the major concepts regarding the cellular and molecular immunology of HFS, with a particular focus on their specific cytokine signatures and physiopathological implications. Based on their molecular and cellular mechanisms, HFS have been classified into intrinsic and extrinsic IL-1β activation disorders or inflammasomopathies, and protein misfolding disorders. This review integrates all recent data in an updated classification of HFS. Highlights • The current review reports a number of advances in the field of inflammatory/immunological mechanisms underlying HFS, and presents all available data regarding the cytokines’ signatures in HFS at the transcriptional, serum and ex vivo levels. • It also integrates recent data in an updated classification of the different HFS in which CAPS, NLRP12AD and FMF were now classified as inflammasomopathies, HIDS/MKD as metabolic dysregulation leading to IL-1β secretion, and TRAPS and the last HFS identified to date, TRAPS11, as protein misfolding disorders. • Cytokine signatures obtained in patients’ cells cultured ex vivo are much more convincing than results obtained at the transcriptional levels or in sera. • Elevated levels of acute phase reactants and pro-inflammatory cytokines in remission periods confirm the involvement of the cytokine network in the inflammatory process and provide evidence for the ongoing subclinical inflammation during asymptomatic periods of HFS. • The marked increase of IL-1β production by LPS-stimulated PBMCs observed in CAPS and NLRP12AD, but also in FMF and MKD, is a hallmark of these disorders. Hereditary fever syndromes (HFS) include a group of disorders characterized by recurrent self-limited episodes of fever accompanied by inflammatory manifestations occurring in the absence of infection or autoimmune reaction. Advances in the genetics of HFS have led to the identification of new gene families and pathways involved in the regulation of inflammation and innate immunity. The key role of several cytokine networks in the pathogenesis of HFS has been underlined by several groups, and supported by the rapid response of patients to targeted cytokine blocking therapies. This can be due to the direct effect of cytokine overproduction or to an absence of receptor antagonist resulting in dysbalance of downstream pro- and anti-inflammatory cytokine networks. The aim of this study was to present an overview and to discuss the major concepts regarding the cellular and molecular immunology of HFS, with a particular focus on their specific cytokine signatures and physiopathological implications. Based on their molecular and cellular mechanisms, HFS have been classified into intrinsic and extrinsic IL-1β activation disorders or inflammasomopathies, and protein misfolding disorders. This review integrates all recent data in an updated classification of HFS. |
Author | Jéru, Isabelle Lecron, Jean-Claude Medlej-Hashim, Myrna Ibrahim, José Noel |
Author_xml | – sequence: 1 fullname: Ibrahim, José Noel – sequence: 2 fullname: Jéru, Isabelle – sequence: 3 fullname: Lecron, Jean-Claude – sequence: 4 fullname: Medlej-Hashim, Myrna |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27916611$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1007_s10067_018_4214_z crossref_primary_10_3390_ijms20236008 crossref_primary_10_1016_j_yexmp_2024_104883 crossref_primary_10_1089_jir_2024_0053 crossref_primary_10_1136_annrheumdis_2019_215258 crossref_primary_10_3390_medsci8030035 crossref_primary_10_1155_2018_1752836 crossref_primary_10_3390_biom11101438 crossref_primary_10_1155_2023_1080495 crossref_primary_10_1186_s13023_024_03098_w crossref_primary_10_1186_s11658_024_00591_9 |
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Keywords | Nuclear factor kappa-light-chain-enhancer of activated B cells TRAPS RANK hematopoietic expression, interferon-inducible nature, and nuclear localization NLRP12-associated disorders AP-1 double stranded DNA TNF CARD myeloid differentiation primary response gene 88 autoinflammatory disorders 3-hydroxy-3-methylglutaryl CoA HFS PI3K type III secretion system Serum PLA 2 tumor necrosis factor receptor superfamily, member 1A PBMC ras-related C3 botulinum toxin substrate 1 FCU polymorphonuclear neutrophils TRIF tumor necrosis factor receptor-associated periodic syndrome DITRA cryopyrin-associated periodic syndromes soluble IL-2 receptor serum smyloid A ASC DIRA TRAPS11 NLR MBL PYD Muckle-Wells syndrome FMF CC erythrocyte sedimentation rate peripheral blood mononuclear cells Transcript ESR apoptosis-associated speck-like protein containing a caspase recruitment domain MKD soluble TNF receptors HIN ex vivo absent in melanoma 2 HIDS tumor necrosis factor adenosine triphosphate ATP MYD88 C-reactive protein IL-1 receptor antagonist ALR ICAM-1 intercellular adhesion molecule 1 LRR mevalonate kinase deficiency FCAS nucleotide-binding oligomerization domain NF-κB activator protein 1 familial cold autoinflammatory syndrome hereditary fever syndromes major histocompatibility complex, MHC class-I-chain-related type A deficit in IL-1 receptor antagonist familial Mediterranean fever RAC1 hyperimmunoglobulinemia D syndrome NOD sTNFr IL-1RA Cytokines pyrin domain PKB TNFRSF1A AIM2–like receptor SAA AIM2 IL-1R1 NOMID ROS phosphoinositide-3-kinase mevalonate kinase dsDNA CRP familial cold urticarial MVK coiled coil chronic infantile neurological cutaneous and articular syndrome AIDs deficit in IL-36 receptor antagonist sIL-2R CINCA reactive oxygen species T3SS IL-1 receptor type I MICA receptor activator of NF-κB TNFRSF11A-associated disorder protein kinase B NLRP12AD leucin rich repeat nod-like receptor phospholipase A 2 MWS HMG-CoA PBMCs caspase recruitment domain TIR-domain-containing adapter-inducing interferon-β danger-associated molecular pattern PMN mannose binding lectin neonatal onset multisystemic inflammatory disease CAPS DAMP PLA2 Hereditary fever syndromes |
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Snippet | Highlights • The current review reports a number of advances in the field of inflammatory/immunological mechanisms underlying HFS, and presents all available... •The current review presents all available data regarding the cytokines’ signatures in HFS at the transcriptional, serum and ex vivo levels.•It also integrates... Hereditary fever syndromes (HFS) include a group of disorders characterized by recurrent self-limited episodes of fever accompanied by inflammatory... |
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SubjectTerms | Advanced Basic Science Animals Cells, Cultured Cryopyrin-Associated Periodic Syndromes - immunology Cryopyrin-Associated Periodic Syndromes - metabolism Cytokines Cytokines - blood Cytokines - genetics Cytokines - immunology ex vivo Familial Mediterranean Fever - immunology Familial Mediterranean Fever - metabolism Hereditary Autoinflammatory Diseases - immunology Hereditary Autoinflammatory Diseases - metabolism Hereditary fever syndromes Humans Immunity, Innate Inflammasomes - metabolism Interleukin-1beta - metabolism Leukocytes, Mononuclear - immunology Lipopolysaccharides - immunology Mevalonate Kinase Deficiency Mice PBMC Serum |
Title | Cytokine signatures in hereditary fever syndromes (HFS) |
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