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 |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Cellular differentiation T cell Short Communication T-Lymphocytes Immunology MKK4 Short Communications T cells Biology Lymphocytic Choriomeningitis Lymphocytic choriomeningitis 03 medical and health sciences Mice 0302 clinical medicine Immune system Immunity medicine Immunology and Allergy Animals Phosphorylation Protein kinase A LCMV Kinase JNK Mitogen-Activated Protein Kinases Cell Differentiation Cell Biology medicine.disease chronic infection MAPK Cell biology Enzyme Activation 030104 developmental biology medicine.anatomical_structure JNK Signal transduction Mitogen-Activated Protein Kinases 030215 immunology |
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 |
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