Organometallic chemistry: Carbon-carbon bonds get a break.

Abstract

IL-33 then stimulates cells to produce TH2-type cytokines such as IL-5 and IL-13 (but not IL-4, the archetypal TH2 cytokine). It also stimulates certain types of progenitor cell to produce the blood-cell growth factor GM-CSF. Rather than being secreted, most IL-33 is targeted to the nucleus of the cell that it is produced by, where it has ill-defined functions that relate to chromatin structure. Because of this intra-nuclear accumulation, IL-33 is released to function as a cytokine only when the cell dies. In this situation, IL-33 may act as an ‘alarmin’ — a substance that signals to the immune system that cell death is occurring and that the organism may be in danger. It is therefore possible that the induction of natural-helper-cell functions by IL-33 is a form of immune response to danger signals that are released when the gut mucosa is attacked by parasites such as helminth worms. The location of natural helper cells potentially allows them to contact a special population of self-renewing B lymphocytes called B1 cells, which reside in the peritoneal cavity. B1 cells make antibodies that are specific for components of commonly encountered microorganisms or self-antigens, including those generated by programmed cell death (apoptosis). It is of considerable interest, therefore, that Moro et al. show that natural helper cells support proliferation of B1 cells, and induce production of antibodies by splenic B cells, particularly IgA antibodies that operate on the mucosal surface. These findings provide a potential answer to the question of how B1 cells are maintained and how they participate in mucosal responses. Last, the stimulation of natural helper cells by IL-33, and their subsequent activation of B cells that neutralize self-antigens arising from cell destruction, may represent a newly discovered but evolutionarily old mechanism for the prevention of autoimmunity. ■ Warren Strober is in the Laboratory of Host Defenses, Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, USA. e-mail: wstrober@niaid.nih.gov

DOI: 10.1038/463435a

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Cite this paper

@article{Goldman2010OrganometallicCC, title={Organometallic chemistry: Carbon-carbon bonds get a break.}, author={Alan S. Goldman}, journal={Nature}, year={2010}, volume={463 7280}, pages={435-6} }