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The report by Wilson and colleagues in this issue of PNAS (1) is one of several in immunology that epitomizes the dictum “to understand the physiology of an immunocyte, learn how this cell regulates its gene expression pattern.” The study of gene regulation, albeit not new, has shifted from its focus on small numbers of model genes under global control mechanisms to a more comprehensive understanding of gene expression changes within a cell. Despite technical challenges, exciting new insights into mechanisms of gene regulation have emerged from these studies. Recent advances in our knowledge of complex genomes and their expressivity, especially those of mice and humans, coupled with the advent of DNA microarray technology have overcome many past limitations. Thus, a comprehensive analysis of gene expression in cells of identical lineage derived under different conditions, healthy or diseased, resting or activated, progenitor/precursor or differentiated/mature, et cetera, is now possible. Reams of data emerge from a microarray analysis at short notice, the sense of which lies in the mind of the beholder. Wilson and colleagues (1) have compared the transcriptional consequences within two human natural T cell (referred to in their paper as Vα24JαQ T cell) clones isolated from monozygotic twins discordant for type 1 diabetes and IL-4 secretion. This comparison entailed a comprehensive analysis of their mRNA expression profile with gene chips. One clone was isolated from the normal twin; it elicits IL-4 on activation through its antigen receptor (Tcr). The other clone was derived from the former's identical but diabetic sibling; it is unable to secrete IL-4 (IL-4-null) on Tcr-mediated activation. The results suggest that the natural T cells from the diabetic twin had dysregulated its genes such that it was polarized toward a Th1 phenotype. Additionally, it had shut off or significantly lowered the expression level of several …

Natural T cells: Cranking up the immune system by prompt cytokine secretion