Targeted tumor necrosis factor receptor I preligand assembly domain improves skin lesions in MRL/lpr mice.

ABSTRACT:

Objective

Skin disease is the second most common manifestation in patients with systemic lupus erythematosus (SLE). Tumor necrosis factor receptor (TNFR) preligand assembly domain (PLAD) has been found to block the effect of TNFalpha, and TNFRI PLAD (p60 PLAD) inhibits inflammatory arthritis. This study was undertaken to investigate whether TNFR PLAD limits inflammatory skin injury in a mouse model of SLE.

Methods

Female MRL/lpr mice received p60 PLAD (100 microg/mouse intraperitoneally), p80 PLAD (100 microg/mouse intraperitoneally), or phosphate buffered saline (100 microl/mouse intraperitoneally) 3 times a week for 26 weeks, starting at age 6 weeks.

Results

Immunohistochemistry studies demonstrated that TNFRI but not TNFRII was dominantly expressed in skin lesions

SUBMITTER: Deng GM 

PROVIDER: S-EPMC2921998 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature