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King, Carolyn G.; Koehli, Sabrina; Hausmann, Barbara; Schmaler, Mathias; Zehn, Dietmar; Palmer, Ed
Immunity (Cambridge, Mass.), 10/2012, Letnik: 37, Številka: 4Journal Article
The strength of interactions between T cell receptors and the peptide-major histocompatibility complex (pMHC) directly modulates T cell fitness, clonal expansion, and acquisition of effector properties. Here we show that asymmetric T cell division is an important mechanistic link between increased signal strength, effector differentiation, and the ability to induce tissue pathology. Recognition of pMHC above a threshold affinity drove responding T cells into asymmetric cell division. The ensuing proximal daughters underwent extensive division and differentiated into short-lived effector cells expressing the integrin VLA-4, allowing the activated T cell to infiltrate and mediate destruction of peripheral target tissues. In contrast, T cells activated by below-threshold antigens underwent symmetric division, leading to abortive clonal expansion and failure to fully differentiate into tissue-infiltrating effector cells. Antigen affinity and asymmetric division are important factors that regulate fate specification in CD8+ T cells and predict the potential of a self-reactive T cell to mediate tissue pathology. ► Antigens above a specific affinity threshold induce asymmetric T cell division ► Proximal daughter T cells efficiently differentiate into tissue-infiltrating SLECs ► Below-threshold antigens induce symmetric division and few tissue infiltrating SLECs
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