Protein T-Bet's Role In Development Of Inflammatory Arthritis

In a study appearing online on January 12 in advance of print publication in the February 2006 issue of the Journal of Clinical Investigation, Laurie Glimcher and colleagues from the Harvard School of Public Health report an essential role for the protein T-bet in the development of inflammatory arthritis.


This protein could provide an attractive new target for therapy for this painful and debilitating condition. Inflammatory arthritis can result when the body's immune system attacks its own healthy tissue and the protein T-bet is a critical regulator of the function of certain immune cells during this response. In their study, Glimcher et al. found that it is the expression of T-bet by dendritic cells, which once activated interact with T and B cells to initiate and shape the immune response, that is critical to the pathology of inflammatory arthritis.


Mice lacking T-bet had markedly reduced joint inflammation and T-bet-deficient mice without T or B cells were essentially resistant to disease. They also found that transfer of normal dendritic cells that make T-bet, but not T-bet-deficient dendritic cells, into mice unable to make T cells, B cells or T-bet, was able to cause inflammatory arthritis. The study shows that the ability of dendritic cells to secrete proinflammatory molecules and to prime T cells to initiate an immune response is compromised in the absence of T-bet. T-bet could provide an attractive new target for therapy in inflammatory arthritis.


TITLE: Transcription factor T-bet regulates inflammatory arthritis through its function in dendritic cells


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Brooke Grindlinger

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Journal of Clinical Investigation

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