Literature DB >> 15086551

Psoriasis-like cutaneous inflammation in mice lacking interleukin-1 receptor antagonist.

Joanna Shepherd1, Matthew C Little, Martin J H Nicklin.   

Abstract

Interleukin-1 receptor antagonist-deficient (Il1rn-/-) BALB/c mice developed inflammation localized to the skin of the ear pinna in 64% of the cases examined. Histopathologically, the disease had many features resembling human psoriasis, suggesting that it might be a useful disease model. The epidermis became thickened and hypertrophic, and expressed the immature keratin, K6, throughout. The stratum corneum showed parakeratotsis. Large epidermal projections formed into a grossly thickened dermis and both tissues were infiltrated by leukocytes. Neutrophil-rich microabscesses formed beneath the stratum corneum. Dendritic cells and activated T cells of both helper classes were identified in both the dermis and epidermis, while a high density of macrophages was seen in the dermis, where mast cells were also prominent. Dense patterns of apparently activated small dermal vessels were seen in the diseased dermis. Cutaneous inflammation, along with arterial inflammation and arthritis, is the third site-specific, inflammatory disease to be found to affect Il1rn-/- BALB/c mice. None of the diseases affected Il1rn-/- C57BL/6. In F2 hybrids of Il1rn-/- BALB/c and C57BL/6, cutaneous inflammation was absent, aortic inflammation was common, and arthritis was rare, indicating that the sets of background modifier genes that cause susceptibility to each disease are not fully overlapping.

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Year:  2004        PMID: 15086551     DOI: 10.1111/j.0022-202X.2004.22305.x

Source DB:  PubMed          Journal:  J Invest Dermatol        ISSN: 0022-202X            Impact factor:   8.551


  32 in total

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6.  Psoriasiform dermatitis is driven by IL-36-mediated DC-keratinocyte crosstalk.

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9.  An autoinflammatory disease due to homozygous deletion of the IL1RN locus.

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10.  Autoinflammatory genes and susceptibility to psoriatic juvenile idiopathic arthritis.

Authors:  T G Day; A V Ramanan; A Hinks; R Lamb; J Packham; C Wise; M Punaro; R P Donn
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