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Martin/Macmillan
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When a T cell meets a dendritic cell that carries an antigen, the meeting activates the T cell to battle pathogens. Less certain is what happens when the dendritic cell doesn't have antigen. Now, two reports bolster the controversial hypothesis that this kind of antigen-free cell-to-cell contact is necessary for the survival of T cells.
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/ p# H' O& t9 a/ W0 o2 n$ cRoland Martin and colleagues of the National Institute of Neurological Disorders and Stroke in Bethesda, MD, found that contact with an antigen-free dendritic cell provokes dramatic changes in human memory T cells〞though not as profound as activation by an antigen. Gene expression shifts, boosting production of cytokines such as interferon gamma, and some T cells begin to divide slowly. Most importantly, the meeting lengthens the life of memory cells, more than doubling the percentage that survive five days in culture.
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Working with naive mouse T cells, a team led by Alain Trautmann of the InstitutCochin de Génétique Moleculaire in Paris, France, saw similar results: greater survival and low-level proliferation in the T cells. "In the normal life of a lymphocyte, it will interact repeatedly with dendritic cells," Trautmann says. "These repeated meetings are essential for survival." To their surprise, the authors also detected a structure known as an immunological synapse at the junction between the cells. The synapse normally forms when a dendritic cell stimulates a T cell, but its formation was thought to require antigen.
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% Y* l$ s* T0 v5 w* `Both groups agree that cellular contact may boost the immune system's readiness in two ways. By stimulating survival and slow reproduction, the interaction may help maintain stocks of T cells. And the low level of stimulation provided by dendritic cells seems to prime lymphocytes for action. However, Martin believes that the work also exposes a possible downside. He thinks that the surge in cytokine production may increase the risk of autoimmune diseases like multiple sclerosis in susceptible individuals. "The interaction may set up a certain environment that is conducive to the pro-inflammatory reactions that you see in autoimmune diseases," he says.
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3 }4 l6 S _( Y& j, yKondo, T., et al. 2001. Nat. Immunol. 2:932–938.
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Revy, P., et al. 2001. Nat. Immunol. 2:925–931.( }' P1 x" e; y+ `
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