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Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Death+Dis 2015 ; 6 (11): e1984- Nephropedia Template TP
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Smad4 represses the generation of memory-precursor effector T cells but is required for the differentiation of central memory T cells #MMPMID26583325
Cao J; Zhang X; Wang Q; Qiu G; Hou C; Wang J; Cheng Q; Lan Y; Han H; Shen H; Zhang Y; Yang X; Shen B; Zhang J
Cell Death Dis 2015[Nov]; 6 (11): e1984- PMID26583325show ga
The transcriptional regulation underlying the differentiation of CD8+ effector and memory T cells remains elusive. Here, we show that 18-month-old mice lacking the transcription factor Smad4 (homolog 4 of mothers against decapentaplegic, Drosophila), a key intracellular signaling effector for the TGF-? superfamily, in T cells exhibited lower percentages of CD44hiCD8+ T cells. To explore the role of Smad4 in the activation/memory of CD8+ T cells, 6- to 8-week-old mice with or without Smad4 in T cells were challenged with Listeria monocytogenes. Smad4 deficiency did not affect antigen-specific CD8+ T-cell expansion but led to partially impaired cytotoxic function. Less short-lived effector T cells but more memory-precursor effector T cells were generated in the absence of Smad4. Despite that, Smad4 deficiency led to reduced memory CD8+ T-cell responses. Further exploration revealed that the generation of central memory T cells was impaired in the absence of Smad4 and the cells showed survival issue. In mechanism, Smad4 deficiency led to aberrant transcriptional programs in antigen-specific CD8+ T cells. These findings demonstrated an essential role of Smad4 in the control of effector and memory CD8+ T-cell responses to infection.