After the demonstration almost 20 years ago that antibodies to CD2 are potent inhibitors of T cell function, this cell surface glycoprotein became one of the most intensively studied of all T cell antigens 1,2,3. The subsequent identification of LFA-3 (CD58) as a ligand for human CD2 led to the demonstration in cell culture experiments that the CD2–CD58 interaction dramatically enhanced T cell antigen recognition 1,2,3. Given this background, it was puzzling that no abnormality in T cell function was observed in the initial experiments on CD2-deficient mice 4,5. A subsequent study did detect some alteration in T cell development and peripheral T cell responses, but the precise nature of the abnormality was unclear 6. Now work by Bachmann and colleagues, described in this issue...

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