The TNF receptor family member CD27 signals to Jun N‐terminal kinase via Traf‐2

• Published in: European journal of immunology Vol. 28; no. 7; pp. 2208 - 2216
• Main Authors: Gravestein, Loes A., Amsen, Derk, Boes, Marianne, Calvo, Concepcion Revilla, Kruisbeek, Ada M., Borst, Jannie
• Format: Journal Article
• Language: English
• Published: Weinheim WILEY‐VCH Verlag GmbH 01.07.1998
• Subjects: Animals; Apoptosis; CD27; COS Cells; Co‐stimulation; JNK; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase 4; Mice; Mice, Inbred C57BL; Mitogen-Activated Protein Kinase Kinases; Protein Kinases - physiology; Proteins - physiology; Receptors, Tumor Necrosis Factor - physiology; T-Lymphocytes - physiology; TNF Receptor-Associated Factor 2; Traf; Tumor Necrosis Factor Receptor Superfamily, Member 7 - physiology
• ISSN: 0014-2980; 1521-4141
• DOI: 10.1002/(SICI)1521-4141(199807)28:07<2208::AID-IMMU2208>3.0.CO;2-L

CD27 is a lymphocyte‐specific member of the TNF receptor (TNFR) family. It is a co‐stimulatory molecule for peripheral T cells, as defined by its ability to enhance the TCR‐induced proliferative response. We show here that CD27 augments TCR‐induced Jun N‐terminal kinase (JNK) activity in primary murine lymph node T cells. To investigate how CD27 couples to JNK, we performed a yeast two hybrid screen with the CD27 cytoplasmic tail. This revealed that CD27 directly associates with Traf‐2. Transfection experiments using dominant negative Traf‐2 indicated that CD27 communicates with JNK via Traf‐2. These findings group CD27 together with other members of the TNFR family, TNFR‐1, −2, CD30 and CD40, which have all been shown to couple to Traf proteins. Since Traf proteins have been reported to initiate an anti‐apoptotic signaling pathway, our data suggest that CD27 not only regulates proliferation, but also survival of T lymphocytes.