The role of MKK4 in T-cell development and immunity to viral infections.
Simon P PrestonMarcel DoerflingerHamish W ScottCody C AllisonMiles HortonJames CooneyMarc PellegriniPublished in: Immunology and cell biology (2020)
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.
Keyphrases
- signaling pathway
- cell death
- induced apoptosis
- endoplasmic reticulum stress
- cell cycle arrest
- oxidative stress
- pi k akt
- sars cov
- protein kinase
- intensive care unit
- liver failure
- metabolic syndrome
- squamous cell carcinoma
- young adults
- drug induced
- respiratory failure
- small molecule
- cell proliferation
- amino acid
- squamous cell