Author/Authors :
Warnatz، نويسنده , , Klaus and Kyburz، نويسنده , , Diego and Brinson، نويسنده , , Diana C. and Lee، نويسنده , , Delphine J. and Von Damm، نويسنده , , Amila and Engelhart، نويسنده , , Michael and Corr، نويسنده , , Maripat and Carson، نويسنده , , Dennis A. and Tighe، نويسنده , , Helen، نويسنده ,
Abstract :
Normal individuals do not express the high-affinity autoantibodies specific for self-IgG (rheumatoid factors, RF) that are commonly seen in rheumatoid arthritis patients. Studies of transgenic mice expressing a human IgM rheumatoid factor have shown that one mechanism by which higher affinity RF B cells are tolerized to IgG is through abortive RF B cell activation followed by deletion in the absence of T cell help. We show that RF B cell deletion occurs through an intrinsic apoptotic mechanism that is independent of the Fas/FasL pathway and does not involve active killing by T cells, as it occurs in RAG-1-deficient RF transgenic mice to the same extent as in the parental RF transgenic line.
