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The role of MKK4 in T‐cell development and immunity to viral infections
Author(s) -
Preston Simon P,
Doerflinger Marcel,
Scott Hamish W,
Allison Cody C,
Horton Miles,
Cooney James,
Pellegrini Marc
Publication year - 2021
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12426
Subject(s) - kinase , microbiology and biotechnology , biology , immune system , t cell , mitogen activated protein kinase , phosphorylation , immunity , immunology
The stress‐activated protein kinases (SAPKs)/c‐Jun‐N‐terminal‐kinases (JNK) are members of the mitogen‐activated protein kinase family. These kinases are responsible for transducing cellular signals through a phosphorylation‐dependent signaling cascade. JNK activation in immune cells can lead to a range of critical cellular responses that include proliferation, differentiation and apoptosis. MKK4 is a SAPK that can activate both JNK1 and JNK2; however, its role in T‐cell development and function has been controversial. Additionally, loss of either JNK1 or JNK2 has opposing effects in the generation of T‐cell immunity to viral infection and cancer. We used mice with a conditional loss of MKK4 in T cells to investigate the in vivo role of MKK4 in T‐cell development and function during lymphocytic choriomeningitis virus (LCMV) infection. We found no physiologically relevant differences in T‐cell responses or immunity to either acute or chronic LCMV in the absence of MKK4.