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Lee and colleagues identify lymph node stromal cells that express peripheral tissue antigens and promote immunological tolerance (p 181; see also News and Views by Zehn & Bevan, p 120). The original image (bottom) shows a cross section of small intestinal villi, with intestinal epithelial cells (red) expressing the basolateral membrane protein A33 antigen and dendritic cells (green) expressing CD11c in the lamina propria. Micrograph by J.-W. Lee. Artwork by Lewis Long.
In honor of the fiftieth anniversary of Frank MacFarlane Burnet's presentation of the clonal selection theory, two of his former staff reminisce about their interactions with this Nobel prize–winning scientist.
There have been enormous advances in the field of immunology over the past 3 decades, and those advances have had a positive effect on many subspecialties of medicine. Opportunities for even more notable advances remain. However, present and projected budget constraints for the National Institutes of Health have created formidable challenges. This commentary addresses the opportunities and challenges for the field of immunology during a period of restricted budgets.
Cell fate 'decisions' involving multipotential progenitors seem to be 'dictated' by threshold activities of lineage-determining transcription factors. Such 'decisions' are now shown to be reinforced by the induction of secondary transcription factors that act in concert with the primary regulators.
Tolerance to self is engendered by multiple mechanisms. Lymph node stromal cells are now found to contribute to self-tolerance by their endogenous expression of peripheral tissue antigens.
New work shows that CARD9, the recently identified member of the caspase recruitment domain–containing family, directly interacts with the cytoplasmic protein Nod2 in the detection of intracellular bacteria.
Regulatory T cells expressing the transcription factor Foxp3 are known to control autoreactivity during and subsequent to the development of the peripheral immune system. New evidence emphasizes the fact that those cells are constant and powerful guardians against the state of 'horror autotoxicus'.
T cell receptor activation requires the membrane-associated guanylate kinase CARMA1. A new study finds that a second such kinase, Dlgh1, is also required specifically for activation of the alternative p38 kinase pathway.