Stimulatory Toll-like receptor 2 suppresses restraint stress-induced immune suppression
| Autor: | James Denney, Deling Yin, Dan Hu, Xiaohua Yang, Manfei Liang, Avani Javer, Ruiliang Zhu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
CD4-Positive T-Lymphocytes
Restraint Physical medicine.medical_specialty medicine.medical_treatment Immunology Blotting Western Stimulation Apoptosis Enzyme-Linked Immunosorbent Assay Peptidoglycan Biology Real-Time Polymerase Chain Reaction Article Mice Immune system Internal medicine medicine Splenocyte In Situ Nick-End Labeling Animals Chronic stress Mice Knockout Toll-like receptor Toll-Like Receptor 2 Cell biology Mice Inbred C57BL TLR2 Cytokine Endocrinology Signal transduction Stress Psychological Signal Transduction |
| Popis: | Stress can enhance or suppress immune functions depending on a variety of factors. Our previous studies observed that Toll-like receptor 2 (TLR2) participates in chronic restraint stress-induced immune dysfunction. However, the mechanism by which TLR2 prevents immune suppression remains elusive. Our investigation found that stimulation of TLR2 by peptidoglycan (PGN) significantly attenuates splenocyte apoptosis and markedly blocks alterations of anti-apoptotic and apoptotic proteins. Activation of TLR2 inhibits chronic stress-reduced phosphorylation of c-Jun N-terminal kinase (JNK) and diminishes chronic stress-induced up-regulation of corticosterone production. Additionally, our data show that chronic stress causes a dramatic decrease of cytokine IL-2 level but an increase of IL-4 and IL-17 in CD4(+) T cells. Interestingly, PGN could block these alterations of cytokine levels. Collectively, our studies demonstrate that stimulation of TLR2 attenuates chronic stress-induced immune suppression by modulating apoptosis-related proteins and immunoregulatory agents. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|