PMID- 18830269
OWN - NLM
STAT- MEDLINE
DCOM- 20090311
LR  - 20220321
IS  - 1523-1747 (Electronic)
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 129
IP  - 3
DP  - 2009 Mar
TI  - Auf1/Hnrnpd-deficient mice develop pruritic inflammatory skin disease.
PG  - 657-70
LID - 10.1038/jid.2008.298 [doi]
AB  - Mice lacking heterogenous nuclear ribonuclear protein D (Hnrnpd), also known as 
      Auf1, a regulator of inflammatory cytokine mRNA stability, develop chronic 
      dermatitis with age that is characterized by pruritus and excoriations. 
      Histological analysis showed marked epidermal acanthosis and spongiosis, 
      neovascularization, and elevated number of inflammatory cells, including T cells, 
      macrophages, neutrophils, mast cells, and eosinophils. Hnrnpd-deficient 
      (Hnrnpd(tm1Rjsc)) mice with dermatitis display elevated serum IgE levels. Lesions 
      in Hnrnpd(tm1Rjsc) mice were associated with a shift towards a Th(2) immune 
      environment. Evaluation of T-cell-mediated skin inflammation by assaying contact 
      hypersensitivity indicated an increased response in Hnrnpd(tm1Rjsc) mice. T cells 
      and macrophages from Hnrnpd(tm1Rjsc) mice demonstrate a number of abnormalities 
      associated with dermatitis, including increased IL2, tumor-necrosis factor-alpha 
      (TNFalpha), and IL1beta production. Finally, many features of spontaneous 
      dermatitis could be recapitulated in experimentally induced lesions by 
      subcutaneous injection of CCL27 and TNF in unaffected Hnrnpd(tm1Rjsc) mice. 
      Collectively, these data highlight the importance of HNRNPD and proper regulation 
      of mRNA stability in the intricate processes of leukocyte recruitment and 
      inflammatory activation within the skin.
FAU - Sadri, Navid
AU  - Sadri N
AD  - Department of Microbiology, New York University School of Medicine, New York, New 
      York 10003, USA.
FAU - Schneider, Robert J
AU  - Schneider RJ
LA  - eng
GR  - R01 GM060428/GM/NIGMS NIH HHS/United States
GR  - R01 GM085693/GM/NIGMS NIH HHS/United States
GR  - T32 AI007180/AI/NIAID NIH HHS/United States
GR  - S10 RR017970/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20081002
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (CCL27 protein, human)
RN  - 0 (Chemokine CCL27)
RN  - 0 (Cytokines)
RN  - 0 (HNRNPD protein, human)
RN  - 0 (Heterogeneous Nuclear Ribonucleoprotein D0)
RN  - 0 (Heterogeneous-Nuclear Ribonucleoprotein D)
RN  - 0 (Hnrpd protein, mouse)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-2)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Chemokine CCL27/metabolism
MH  - Cytokines/metabolism
MH  - Dermatitis/metabolism
MH  - Female
MH  - Heterogeneous Nuclear Ribonucleoprotein D0
MH  - Heterogeneous-Nuclear Ribonucleoprotein D/*genetics/*physiology
MH  - Inflammation/*metabolism
MH  - Interleukin-1beta/metabolism
MH  - Interleukin-2/metabolism
MH  - Macrophages/metabolism
MH  - Male
MH  - Mice
MH  - Pruritus/*metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC4074411
MID - NIHMS584766
COIS- CONFLICTS OF INTEREST The authors state no conflict of interest.
EDAT- 2008/10/03 09:00
MHDA- 2009/03/12 09:00
PMCR- 2014/06/28
CRDT- 2008/10/03 09:00
PHST- 2008/10/03 09:00 [pubmed]
PHST- 2009/03/12 09:00 [medline]
PHST- 2008/10/03 09:00 [entrez]
PHST- 2014/06/28 00:00 [pmc-release]
AID - S0022-202X(15)34262-7 [pii]
AID - 10.1038/jid.2008.298 [doi]
PST - ppublish
SO  - J Invest Dermatol. 2009 Mar;129(3):657-70. doi: 10.1038/jid.2008.298. Epub 2008 
      Oct 2.