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This portfolio of published work represents a discourse on Michael Fordham's model of development that extended Jung's theory to infancy and childhood. The papers were published over two decades and indicate how infant research, ideas from related fields and the author's own clinical and observational work have contributed to her understanding of development. The framework for her thinking has throughout been Fordham's model. In this essay the author contends that what she has learned from research and her own experience adds new contributions to the model, based on data for the most part not available to Fordham. The portfolio of papers is introduced by an essay comprising Part I. It begins with an account of the author's professional life and clinical experience pertinent to the study. Next there is a substantial section on Fordham ' s theoretical model and links he established with Kleinian and post-Kleinian thought. This exposition is followed by a section on the main sources for the author's work. Following this she proposes five areas that she considers to be her original contributions to the model: identifying and defining the features of massive surges of deintegration in the first year; identifying a period of primary self functioning; new considerations concerning the active participation of the infant in development; identifying precursors to projective and introjective identification, and symbol formation. Part II contains nine papers, virtually all of which are theoretical and include clinical work and infant research and observation. They are divided into three sections: 'Theory ', which are predominantly theoretical and ain1ed at making a theoretical point; 'Exp lications ', which aim to elucidate concepts and dynamics comprising the model; and 'Extensions', which are those papers explicitly or implicitly containing the author's new links and ideas that add form and content to the model.

T cells develop into two major populations distinguished by their T cell receptor (TCR) chains. Cells with the αβ TCR generally express CD4 or CD8 lineage markers and mostly fall into helper or cytotoxic/effector subsets. Cells expressing the alternate γδ TCR in humans generally do not express lineage markers, do not require MHC for antigen presentation, and recognize nonpeptidic antigens. We are interested in the dominant Vγ2Vδ2+ T cell subset in human peripheral blood and the control of effector function in this population. We review the literature on γδ T cell generation and repertoire selection, along with recent work on CD56 expression and defining a cytotoxic/effector lineage within the phosphoantigen-reactive Vγ2Vδ2 cells. A unique mechanism for MHC-independent repertoire selection is linked to the control of effector function that is vital to the role for γδ T cells in tumor surveillance. Better understanding of these mechanisms will improve our ability to exploit this population for tumor immunotherapy.