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JCI early table of contents for Jan. 25, 2013


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iRHOM2: the newest gadget in rheumatoid arthritis

Rheumatoid arthritis (RA) is an inflammatory joint disorder that gradually destroys cartilage, causing loss of joint function and mobility. TNF is a protein that mediates inflammation in RA. TNF is generated when an enzyme known as TACE release TNF from immune cells. Therapeutic targeting of TACE could reduce TNF, but TACE is also important to other physiological processes, making it a poor drug target. In this issue of the Journal of Clinical Investigation, Carl Blobel and colleagues at Weill Cornell University demonstrated that the protein iRHOM2 in immune cells. Blobel and colleagues found that inhibition of iRHOM2 selectively blocked TACE activity in immune cells without disrupting other functions. Additionally, mice lacking iRHOM2 were protected from inflammatory arthritis. In a companion commentary, Stefan Lichtenthaler of the German Center for Neurodegenerative Diseases in Munich Germany discusses iRHOM2's potential as a therapeutic target in RA.

iRHOM2 is a critical pathogenic mediator of inflammatory arthritis

Carl Blobel
Weill Medical College of Cornell University, New York, NY, USA
Phone: 212-606-1429; Fax: 212-774-2560; E-mail:

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iRhom2 takes control of rheumatoid arthritis

Stefan Lichtenthaler
German Center for Neurodegene

Contact: Jillian Hurst
Journal of Clinical Investigation

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