PMID- 34939663
OWN - NLM
STAT- MEDLINE
DCOM- 20220504
LR  - 20220818
IS  - 1365-2133 (Electronic)
IS  - 0007-0963 (Print)
IS  - 0007-0963 (Linking)
VI  - 186
IP  - 5
DP  - 2022 May
TI  - The biological basis of disease recurrence in psoriasis: a historical perspective 
      and current models.
PG  - 773-781
LID - 10.1111/bjd.20963 [doi]
AB  - A key challenge in psoriasis therapy is the tendency for lesions to recur in 
      previously affected anatomical locations after treatment discontinuation 
      following lesion resolution. Available evidence supports the concept of a 
      localized immunological 'memory' that persists in resolved skin after complete 
      disappearance of visible inflammation, as well as the role of a specific 
      subpopulation of T cells characterized by the dermotropic CCR4(+) phenotype and 
      forming a local memory. Increasing knowledge of the interleukin (IL)-23/T helper 
      17 (Th17) cell pathway in psoriasis immunopathology is pointing away from the 
      historical classification of psoriasis as primarily a Th1-type disease. Research 
      undertaken from the 1990s to the mid-2000s provided evidence for the existence of 
      a large population of CD8(+) and CD4(+) tissue-resident memory T cells in 
      resolved skin, which can initiate and perpetuate immune responses of psoriasis in 
      the absence of T-cell recruitment from the blood. Dendritic cells (DCs) are 
      antigen-presenting cells that contribute to psoriasis pathology via the secretion 
      of IL-23, the upstream regulator of Th17 cells, while plasmacytoid DCs are 
      involved via IL-36 signalling and type I interferon activation. Overall, the 
      evidence discussed in this review indicates that IL-23-driven/IL-17-producing T 
      cells play a critical role in psoriasis pathology and recurrence, making these 
      cytokines logical therapeutic targets. The review also explains the clinical 
      efficacy of IL-17 and IL-23 receptor blockers in the treatment of psoriasis.
CI  - (c) 2021 British Association of Dermatologists.
FAU - Puig, Lluis
AU  - Puig L
AUID- ORCID: 0000-0001-6083-0952
AD  - Department of Dermatology, Hospital de la Santa Creu i Sant Pau, Barcelona, 
      Spain.
FAU - Costanzo, Antonio
AU  - Costanzo A
AD  - Unit of Dermatology, IRCCS Humanitas Research Hospital, Rozzano, Milan, Italy.
AD  - Department of Biomedical Sciences, Humanitas University, Pieve Emanuele, Milan, 
      Italy.
FAU - Munoz-Elias, Ernesto J
AU  - Munoz-Elias EJ
AD  - Department of Immunology - Translational Biology, Biomarkers & Early Development, 
      Janssen Research & Development, CA/Spring House, La Jolla, PA, USA.
FAU - Jazra, Maria
AU  - Jazra M
AD  - Medical Affairs, Janssen-Cilag, Paris, France.
FAU - Wegner, Sven
AU  - Wegner S
AD  - Medical Affairs, Janssen-Cilag GmbH, Neuss, Germany.
FAU - Paul, Carle F
AU  - Paul CF
AUID- ORCID: 0000-0003-0165-5263
AD  - Department of Dermatology, Hopital Larrey, CHU Toulouse, Toulouse, France.
FAU - Conrad, Curdin
AU  - Conrad C
AD  - Department of Dermatology, University Hospital CHUV, Lausanne, Switzerland.
LA  - eng
GR  - Janssen Pharmaceutica NV/
PT  - Journal Article
PT  - Review
PL  - England
TA  - Br J Dermatol
JT  - The British journal of dermatology
JID - 0004041
RN  - 0 (Interleukin-17)
RN  - 0 (Interleukin-23)
SB  - IM
MH  - Humans
MH  - *Interleukin-17
MH  - Interleukin-23
MH  - *Psoriasis/drug therapy
MH  - Skin/pathology
MH  - Th17 Cells
PMC - PMC9374062
EDAT- 2021/12/24 06:00
MHDA- 2022/05/06 06:00
PMCR- 2022/08/12
CRDT- 2021/12/23 08:48
PHST- 2021/11/23 00:00 [revised]
PHST- 2021/07/09 00:00 [received]
PHST- 2021/12/17 00:00 [accepted]
PHST- 2021/12/24 06:00 [pubmed]
PHST- 2022/05/06 06:00 [medline]
PHST- 2021/12/23 08:48 [entrez]
PHST- 2022/08/12 00:00 [pmc-release]
AID - BJD20963 [pii]
AID - 10.1111/bjd.20963 [doi]
PST - ppublish
SO  - Br J Dermatol. 2022 May;186(5):773-781. doi: 10.1111/bjd.20963.