PMID- 32259663
OWN - NLM
STAT- MEDLINE
DCOM- 20210510
LR  - 20210510
IS  - 1532-2777 (Electronic)
IS  - 0306-9877 (Linking)
VI  - 139
DP  - 2020 Jun
TI  - New aspect of allergic contact dermatitis, an inflammatory skin disorder mediated 
      by mast cells: Can IL-38 help?
PG  - 109687
LID - S0306-9877(20)30351-0 [pii]
LID - 10.1016/j.mehy.2020.109687 [doi]
AB  - Atopic dermatitis (AD) is an inflammatory reaction of the skin that can occur in 
      several parts of the body and can be provoked or exacerbated by food and/or 
      environmental compounds. Allergic contact dermatitis (ACD) is a potential 
      enhancer of AD, and an epidermal barrier breaker which induces greater 
      penetration of allergens and other compounds. ACD presents an eczematous rash, 
      red and itchy, with inflammation mediated by cytokines. ACD is an immunological 
      disorder caused by contact with an allergic substance (haptens) that involves 
      immunotoxicity, irritation and inflammation. Mast cells (MCs) are important 
      immune cells that intervene, as effector cells, in allergic and anaphylactic 
      reactions, asthma, autoimmune diseases and cancer. In dermatitis, activated MCs 
      release inflammatory chemical mediators and secrete pro-inflammatory cytokines, 
      including interleukin (IL)-1, TNF, and IL-33. In addition, IL-1 activates MCs to 
      generate a number of cytokines and chemokines, which aggravate inflammation. 
      IL-38 cytokine, an IL-1 family member, is secreted by activated immune cells, 
      including macrophages and lymphocytes, and possesses anti-inflammatory activity. 
      IL-38, by binding IL-36 receptor (IL-36R), provokes suppression of inflammation 
      in many immune diseases. In particular, IL-38 inhibits the generation of IL-1, 
      IL-6 and IL-8 along with other cytokines/chemokines. Here, we hypothesize for the 
      first time that IL-38 may suppresses the inflammatory response in dermatitis, 
      exerting beneficial therapeutic effect.
CI  - Copyright (c) 2020 Elsevier Ltd. All rights reserved.
FAU - Lauritano, Dorita
AU  - Lauritano D
AD  - Medicine and Surgery Department, Centre of Neuroscience of Milan, University of 
      Milan-Bicocca, Italy.
FAU - Ronconi, Gianpaolo
AU  - Ronconi G
AD  - Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome, Italy.
FAU - Caraffa, Alessandro
AU  - Caraffa A
AD  - School of Pharmacy, University of Camerino, Camerino, Italy.
FAU - Enrica Gallenga, Carla
AU  - Enrica Gallenga C
AD  - Department of Biomedical Sciences and Specialist Surgery, Section of 
      Ophthalmology, University of Ferrara, Ferrara, Italy.
FAU - Kritas, Spyros K
AU  - Kritas SK
AD  - Department of Microbiology and Infectious Diseases, School of Veterinary 
      Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.
FAU - Di Emidio, Paolo
AU  - Di Emidio P
AD  - Department of Maxillofacial, Teramo Hospital, Italy.
FAU - Martinotti, Stefano
AU  - Martinotti S
AD  - Department of Medical, Oral and Biotechnological Sciences, University "G. 
      d'Annunzio" of Chieti-Pescara, Chieti, Italy.
FAU - Tete, Giulia
AU  - Tete G
AD  - DDS, Graduate School, Oral Surgery, Vita-Salute San Raffaele University, Milan, 
      Italy.
FAU - Ross, Rhiannon
AU  - Ross R
AD  - University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA 19104, 
      USA.
FAU - Conti, Pio
AU  - Conti P
AD  - Postgraduate Medical School, University of Chieti, Chieti, Italy. Electronic 
      address: pconti@unich.it.
LA  - eng
PT  - Journal Article
DEP - 20200321
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Cytokines)
RN  - 0 (IL-38 protein, human)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukins)
SB  - IM
MH  - *Cytokines
MH  - *Dermatitis, Allergic Contact
MH  - Humans
MH  - Interleukin-1
MH  - Interleukins
MH  - *Mast Cells
MH  - Skin
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2020/04/08 06:00
MHDA- 2021/05/11 06:00
CRDT- 2020/04/08 06:00
PHST- 2020/03/03 00:00 [received]
PHST- 2020/03/20 00:00 [accepted]
PHST- 2020/04/08 06:00 [pubmed]
PHST- 2021/05/11 06:00 [medline]
PHST- 2020/04/08 06:00 [entrez]
AID - S0306-9877(20)30351-0 [pii]
AID - 10.1016/j.mehy.2020.109687 [doi]
PST - ppublish
SO  - Med Hypotheses. 2020 Jun;139:109687. doi: 10.1016/j.mehy.2020.109687. Epub 2020 
      Mar 21.