The RNA-Binding Protein HuR Posttranscriptionally Regulates IL-2 Homeostasis and CD4 + Th2 Differentiation
Posttranscriptional gene regulation by RNA-binding proteins, such as HuR ( ), fine-tune gene expression in T cells, leading to powerful effects on immune responses. HuR can stabilize target mRNAs and/or promote translation by interacting with their 3' untranslated region adenylate and uridylate...
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| Veröffentlicht in: | ImmunoHorizons 2017-08, Vol.1 (6), p.109-123 |
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| creator | Techasintana, Patsharaporn Ellis, Jason S Glascock, Jacqueline Gubin, Matthew M Ridenhour, Suzanne E Magee, Joseph D Hart, Marcia L Yao, Peng Zhou, Hao Whitney, Maryln S Franklin, Craig L Martindale, Jennifer L Gorospe, Myriam Davis, Wade J Fox, Paul L Li, Xiaoxia Atasoy, Ulus |
| description | Posttranscriptional gene regulation by RNA-binding proteins, such as HuR (
), fine-tune gene expression in T cells, leading to powerful effects on immune responses. HuR can stabilize target mRNAs and/or promote translation by interacting with their 3' untranslated region adenylate and uridylate-rich elements. It was previously demonstrated that HuR facilitates Th2 cytokine expression by mRNA stabilization. However, its effects upon IL-2 homeostasis and CD4
Th2 differentiation are not as well understood. We found that optimal translation of
(CD25) required interaction of its mRNA with HuR. Conditional HuR knockout in CD4
T cells resulted in loss of IL-2 homeostasis and defects in JAK-STAT signaling, Th2 differentiation, and cytokine production. HuR-knockout CD4
T cells from OVA-immunized mice also failed to proliferate in response to Ag. These results demonstrate that HuR plays a pivotal role in maintaining normal IL-2 homeostasis and initiating CD4
Th2 differentiation. |
| doi_str_mv | 10.4049/immunohorizons.1700017 |
| format | Article |
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), fine-tune gene expression in T cells, leading to powerful effects on immune responses. HuR can stabilize target mRNAs and/or promote translation by interacting with their 3' untranslated region adenylate and uridylate-rich elements. It was previously demonstrated that HuR facilitates Th2 cytokine expression by mRNA stabilization. However, its effects upon IL-2 homeostasis and CD4
Th2 differentiation are not as well understood. We found that optimal translation of
(CD25) required interaction of its mRNA with HuR. Conditional HuR knockout in CD4
T cells resulted in loss of IL-2 homeostasis and defects in JAK-STAT signaling, Th2 differentiation, and cytokine production. HuR-knockout CD4
T cells from OVA-immunized mice also failed to proliferate in response to Ag. These results demonstrate that HuR plays a pivotal role in maintaining normal IL-2 homeostasis and initiating CD4
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Th2 differentiation are not as well understood. We found that optimal translation of
(CD25) required interaction of its mRNA with HuR. Conditional HuR knockout in CD4
T cells resulted in loss of IL-2 homeostasis and defects in JAK-STAT signaling, Th2 differentiation, and cytokine production. HuR-knockout CD4
T cells from OVA-immunized mice also failed to proliferate in response to Ag. These results demonstrate that HuR plays a pivotal role in maintaining normal IL-2 homeostasis and initiating CD4
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Th2 differentiation are not as well understood. We found that optimal translation of
(CD25) required interaction of its mRNA with HuR. Conditional HuR knockout in CD4
T cells resulted in loss of IL-2 homeostasis and defects in JAK-STAT signaling, Th2 differentiation, and cytokine production. HuR-knockout CD4
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| title | The RNA-Binding Protein HuR Posttranscriptionally Regulates IL-2 Homeostasis and CD4 + Th2 Differentiation |
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