CAML is a p56Lck-interacting protein that is required for thymocyte development

David D. Tran, Contessa E. Edgar, Karin L. Heckman, Shari L. Sutor, Catherine J. Huntoon, Jan Van Deursen, David L. McKean, Richard J. Bram

Research output: Contribution to journalArticlepeer-review

31 Scopus citations


Calcium modulating cyclophilin ligand (CAML) is a ubiquitously expressed protein implicated in T cell signaling, although its mechanism and physiologic role in the immune system are unknown. We show here that CAML is essential for peripheral T cell development. Inactivation of CAML in mouse thymocytes lowered the numbers of double-positive and single-positive thymocytes, concomitant with reduced positive and enhanced negative selection. We found that CAML interacts with p56Lck and appears to regulate subcellular localization of the kinase in both resting and T cell receptor (TCR)-stimulated cells. CAML-deficient cells displayed enhanced p56lck and ZAP-70 phosphorylation and increased IL2 production and cell death after TCR stimulation, suggesting that CAML may act as a negative regulator of p56lck. Our data establish a novel role for CAML as an essential mediator of T cell survival during thymopoiesis and indicate that its loss deregulates p56Lck signaling.

Original languageEnglish (US)
Pages (from-to)139-152
Number of pages14
Issue number2
StatePublished - Aug 2005

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases


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