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TRANCE–RANK, a New Signal Pathway Involved in Lymphocyte Development and T Cell Activation

Journal of Experimental Medicine
The Rockefeller University Press
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  • Biology


99-C004 1017 J. Exp. Med. Ó The Rockefeller University Press • 0022-1007/99/04/1017/04 $2.00 Volume 189, Number 7, April 5, 1999 1017–1020 Commentary TRANCE–RANK, a New Signal Pathway Involved in Lymphocyte Development and T Cell Activation By E. Allison Green * and Richard A. Flavell * ‡ From the * Section of Immunobiology and ‡ Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510 A lmost a decade ago, major advancements in our un- derstanding of the cell–cell interactions that were crit- ically involved in the regulation of the immune response were achieved when it was established that T cell activation not only required a signal through the T cell receptor but also a second signal generated by the interaction of costim- ulatory molecules CD80 and CD86 on the surface of APCs and CD28 or CTLA-4 on T cells (1). Since then, identifi- cation of other molecular interactions that are important in regulating the immune response has increased dramatically, elucidating signals that enhance stable cellular interactions between APCs and T cells as well as apoptotic signals that regulate survival of either the APC or the T cell (2, 3). One molecular interaction that has received enormous attention is that between CD40 on APCs and CD154 on T cells (re- viewed in 4). CD40–CD154 signals are a vital component in the generation of humoral immunity, as exemplified by murine models in which blockade of CD40–CD154 sig- nals, either by antibodies or the creation of a null mutation in CD154, abrogates development of B cell responses to thymus-dependent antigens (5, 6). Signals through CD40 can also influence the activity of other APCs, in particular dendritic cells (DCs), leading to the upregulation of adhe- sion and costimulatory molecules (7, 8), increased accumu- lation of peptide–MHC complexes on DC surfaces, and the generat

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