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This paper reviews some of the results and the speculations presented at the Torino CD38 Meeting in June, 2006 and focused on CD38 and CD157 seen as a family of molecules acting as surface receptors of immune cells. This partisan view was adopted in the attempt to combine the enzymatic functions with what the immunologists consider key functions in different cell models. At the moment, it is unclear whether the two functions are correlated, indifferent, or independent. Here we present conclusions inferred exclusively on human cell models, namely T and B lymphocytes, dendritic cells, and granulocytes. As an extra analytical tool, we try to follow in the history of life when the enzymatic and receptorial functions were generated, mixing ontogeny, membrane localization, and cell anchorage. [ABSTRACT FROM AUTHOR]

Negative selection eliminates thymocytes bearing autoreactive T cell receptors (TCR) via an apoptotic mechanism. We have cloned an inhibitor of NF-κB, IκBNS, which is rapidly expressed upon TCR-triggered but not dexamethasone- or γ irradiation-stimulated thymocyte death. The predicted protein contains seven ankyrin repeats and is homologous to IκB family members. In class I and class II MHC-restricted TCR transgenic mice, transcription of IκBNS is stimulated by peptides that trigger negative selection but not by those inducing positive selection (i.e., survival) or nonselecting peptides. IκBNS blocks transcription from NF-κB reporters, alters NF-κB electrophoretic mobility shifts, and interacts with NF-κB proteins in thymic nuclear lysates following TCR stimulation. Retroviral transduction of IκBNS in fetal thymic organ culture enhances TCR-triggered cell death consistent with its function in selection. [Copyright &y& Elsevier]