The role of MKK4 in T‐cell development and immunity to viral infections

Autor: Cody C. Allison, Marc Pellegrini, Miles B Horton, Simon Preston, Marcel Doerflinger, James P Cooney, Hamish W Scott
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Immunology and Cell Biology
ISSN: 1440-1711
0818-9641
Popis: 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.
MKK4 is a stress‐activated protein kinase that can activate both JNK1 and JNK2; however, its role in T‐cell development and function has been controversial. 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 infection. Contrary to previous reports, we found that T‐cell development and expansion during both acute and chronic viral infection was unperturbed by the loss of MKK4.
Databáze: OpenAIRE