PMID- 32422017
OWN - NLM
STAT- MEDLINE
DCOM- 20200904
LR  - 20200904
IS  - 1040-8401 (Print)
IS  - 1040-8401 (Linking)
VI  - 39
IP  - 5
DP  - 2019
TI  - Pathogenesis of Psoriatic Arthritis.
PG  - 361-377
LID - 10.1615/CritRevImmunol.2020033243 [doi]
AB  - Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy involving 
      synovial and entheseal structures, associated with psoriasis or similar 
      conditions. The etiopathogenetic mechanisms underlying PsA remain unclarified. 
      The most accredited hypothesis involves a complex interaction among genetic, 
      environmental, and immunological factors. Environmental agents, particularly 
      trauma, mechanical stress, and smoke have been cited as possible factors in 
      triggering the disease in genetically predisposed subjects. Like other forms of 
      spondyloarthropathies, PsA shows several genetic associations with the major 
      histocompatibility complex (MHC) class I alleles located on chromosome 6p21.3, 
      particularly the human leukocyte antigen (HLA)-B27 in axial phenotypes. Recent 
      studies have demonstrated that the most common epigenetic mechanisms that 
      regulate gene expression in PsA are represented by DNA methylation, parent of 
      origin effect or genomic imprinting, expression or activity of epigenetic 
      modifying enzymes, and RNA interference (RNAi) by microRNAs (miRNAs). The 
      mechanisms underlying PsA pathogenesis activate the innate and adaptive immune 
      system and overexpression of TNF associated with amplification of the IL-23/IL-17 
      axis. In recent years, more PsA susceptibility genes and epigenetic mechanisms 
      have been identified. Advances in the knowledge of innate and adaptive immune 
      mechanisms underlying PsA have contributed to a better understanding of the 
      heterogeneous clinical expression of the disease and, thus, to therapy 
      strategies. The complexity of the pathogenetic aspects involving multiple 
      cytokines, cell lines, and molecules needs to be further investigated to advance 
      personalized therapeutic strategies and to improve outcomes of patients affected 
      by PsA.
FAU - Caso, Francesco
AU  - Caso F
AD  - Rheumatology Unit, Department of Clinical Medicine and Surgery, School of 
      Medicine, University Federico II of Naples, Via S. Pansini 5, 80131, Naples, 
      Italy.
FAU - Costa, Luisa
AU  - Costa L
AD  - Rheumatology Unit, Department of Clinical Medicine and Surgery, School of 
      Medicine, University Federico II of Naples, Via S. Pansini 5, 80131, Naples, 
      Italy.
FAU - Chimenti, Maria Sole
AU  - Chimenti MS
AD  - Rheumatology, Allergology and Clinical Immunology, University of Rome Tor 
      Vergata, Rome, Italy.
FAU - Navarini, Luca
AU  - Navarini L
AD  - Unit of Allergology, Clinical Immunology and Rheumatology, Universita Campus 
      Bio-Medico di Roma, Rome, Italy.
FAU - Punzi, Leonardo
AU  - Punzi L
AD  - Department of Clinical Medicine DIMED, University of Padova, Padua, Italy; Centre 
      for Gout and Metabolic Bone and Joint Diseases, Rheumatology, SS Giovanni and 
      Paolo, Venice, Italy.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Crit Rev Immunol
JT  - Critical reviews in immunology
JID - 8914819
RN  - 0 (HLA-B27 Antigen)
RN  - 0 (Interleukin-17)
RN  - 0 (Interleukin-23)
SB  - IM
MH  - Arthritis, Psoriatic/*genetics/immunology
MH  - Biological Therapy
MH  - Epigenesis, Genetic
MH  - Genetic Predisposition to Disease
MH  - HLA-B27 Antigen/*genetics
MH  - Humans
MH  - Interleukin-17/*metabolism
MH  - Interleukin-23/metabolism
MH  - Precision Medicine
MH  - Signal Transduction
EDAT- 2019/01/01 00:00
MHDA- 2020/09/05 06:00
CRDT- 2020/05/19 06:00
PHST- 2020/05/19 06:00 [entrez]
PHST- 2019/01/01 00:00 [pubmed]
PHST- 2020/09/05 06:00 [medline]
AID - 2a7315b36e01386e,41905f076fae9cd7 [pii]
AID - 10.1615/CritRevImmunol.2020033243 [doi]
PST - ppublish
SO  - Crit Rev Immunol. 2019;39(5):361-377. doi: 10.1615/CritRevImmunol.2020033243.