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Early studies using genetic models, alongside analyses of human patients with mutations suggested that NF-B signaling played a role in establishing long-term protective T cell memory pools (159, 160), However, the lack of inducible T cell-restricted NF-B models has made it difficult to determine whether the observed defects in memory T cell levels result from early issues with T cell priming or proliferation, or from later problems in differentiation and survival

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MiR-429 Prohibited NF-b Signalling to Alleviate Contrast-Induced Acute Kidney Injury via Targeting PDCD4

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