PMID- 30417427
OWN - NLM
STAT- MEDLINE
DCOM- 20200622
LR  - 20210108
IS  - 1600-0625 (Electronic)
IS  - 0906-6705 (Linking)
VI  - 28
IP  - 2
DP  - 2019 Feb
TI  - IL-36 receptor antagonistic antibodies inhibit inflammatory responses in 
      preclinical models of psoriasiform dermatitis.
PG  - 113-120
LID - 10.1111/exd.13841 [doi]
AB  - Psoriasis vulgaris (PV) results from activation of IL-23/Th17 immune pathway and 
      is further amplified by cytokines/chemokines from skin cells. Among skin-derived 
      pro-inflammatory cytokines, IL-36 family members are highly upregulated in PV 
      patients and play a critical role in general pustular psoriasis. However, there 
      is limited data showing crosstalk between the IL-23 and IL-36 pathways in PV. 
      Herein, potential attenuation of skin inflammation in the IL-23-induced mouse 
      model of psoriasiform dermatitis by functional inhibition of IL-36 receptor 
      (IL-36R) was interrogated. Anti-mouse IL-36R monoclonal antibodies (mAbs) were 
      generated and validated in vitro by inhibiting IL-36alpha-induced secretion of CXCL1 
      from NIH 3T3 cells. Antibody target engagement was demonstrated by inhibition of 
      CXCL1 production in a novel acute model of IL-36alpha systemic injection in mice. In 
      addition, anti-IL-36R mAbs inhibited tissue inflammation and inflammatory gene 
      expression in an IL-36alpha ear injection model of psoriasiform dermatitis 
      demonstrating engagement of the target in the ear skin. To elucidate the possible 
      role of IL-36 signalling in IL-23/Th17 pathway, the ability of anti-IL-36R mAbs 
      to inhibit skin inflammation in an IL-23 ear injection model was assessed. 
      Inhibiting the IL-36 pathway resulted in significant attenuation of skin 
      thickening and psoriasis-relevant gene expression. Taken together, these data 
      suggest a role for IL-36 signalling in the IL-23/Th17 signalling axis in PV.
CI  - (c) 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Su, Zhi
AU  - Su Z
AUID- ORCID: 0000-0002-4763-3361
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Paulsboe, Stephanie
AU  - Paulsboe S
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Wetter, Joseph
AU  - Wetter J
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Salte, Katherine
AU  - Salte K
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Kannan, Arun
AU  - Kannan A
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Mathew, Sheeba
AU  - Mathew S
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Horowitz, Amanda
AU  - Horowitz A
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Gerstein, Clare
AU  - Gerstein C
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Namovic, Marian
AU  - Namovic M
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Todorovic, Viktor
AU  - Todorovic V
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Seagal, Jane
AU  - Seagal J
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Edelmayer, Rebecca M
AU  - Edelmayer RM
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Viner, Michelle
AU  - Viner M
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Rinaldi, Lisa
AU  - Rinaldi L
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Zhou, Li
AU  - Zhou L
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Leys, Laura
AU  - Leys L
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Huang, Susan
AU  - Huang S
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Wang, Leyu
AU  - Wang L
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Sadhukhan, Ramkrishna
AU  - Sadhukhan R
AD  - Abbvie Bioresearch Center, AbbVie Inc., Worcester, Massachusetts.
FAU - Honore, Prisca
AU  - Honore P
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - McGaraughty, Steve
AU  - McGaraughty S
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
FAU - Scott, Victoria E
AU  - Scott VE
AD  - Dermatology Discovery, AbbVie Inc., North Chicago, Illinois.
LA  - eng
PT  - Journal Article
DEP - 20181221
PL  - Denmark
TA  - Exp Dermatol
JT  - Experimental dermatology
JID - 9301549
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Cxcl1 protein, mouse)
RN  - 0 (Cytokines)
RN  - 0 (Il1rl2 protein, rat)
RN  - 0 (Il36a protein, rat)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-23)
RN  - 0 (Interleukins)
RN  - 0 (Ligands)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (interleukin 1F6, mouse)
RN  - 0 (interleukin-36 receptor, mouse)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/*immunology/therapeutic use
MH  - Chemokine CXCL1/metabolism
MH  - Cytokines/metabolism
MH  - Dermatitis/*immunology/therapy
MH  - Disease Models, Animal
MH  - Female
MH  - Gene Expression Profiling
MH  - Inflammation/*immunology/metabolism
MH  - Interleukin-1/immunology
MH  - Interleukin-23/pharmacology
MH  - Interleukins/*immunology
MH  - Ligands
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - NIH 3T3 Cells
MH  - Psoriasis/*immunology/therapy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Interleukin/*antagonists & inhibitors/immunology
MH  - Receptors, Interleukin-1/immunology
MH  - Signal Transduction
MH  - Skin/metabolism/pathology
MH  - Th17 Cells/cytology
OTO - NOTNLM
OT  - IL-23
OT  - IL-36
OT  - IL-36 receptor antibody
OT  - inflammation
OT  - psoriasis
EDAT- 2018/11/13 06:00
MHDA- 2020/06/23 06:00
CRDT- 2018/11/13 06:00
PHST- 2018/06/20 00:00 [received]
PHST- 2018/11/02 00:00 [revised]
PHST- 2018/11/06 00:00 [accepted]
PHST- 2018/11/13 06:00 [pubmed]
PHST- 2020/06/23 06:00 [medline]
PHST- 2018/11/13 06:00 [entrez]
AID - 10.1111/exd.13841 [doi]
PST - ppublish
SO  - Exp Dermatol. 2019 Feb;28(2):113-120. doi: 10.1111/exd.13841. Epub 2018 Dec 21.