التفاصيل البيبلوغرافية
| العنوان: |
CD4 T cells control development and maintenance of brain-resident CD8 T cells during polyomavirus infection. |
| المؤلفون: |
Mockus, Taryn E., Shwetank, null, Lauver, Matthew D., Ren, Heather M., Netherby, Colleen S., Salameh, Tarik, Kawasawa, Yuka Imamura, Yue, Feng, Broach, James R., Lukacher, Aron E. |
| المصدر: |
PLoS Pathogens; 10/29/2018, Vol. 14 Issue 10, p1-25, 25p |
| مصطلحات موضوعية: |
CD4 lymphocyte count, POLYOMAVIRUS diseases, T cells, LYMPHOCYTES, VIRUS diseases |
| مستخلص: |
Tissue-resident memory CD8 T (TRM) cells defend against microbial reinfections at mucosal barriers; determinants driving durable TRM cell responses in non-mucosal tissues, which often harbor opportunistic persistent pathogens, are unknown. JC polyomavirus (JCPyV) is a ubiquitous constituent of the human virome. With altered immunological status, JCPyV can cause the oft-fatal brain demyelinating disease progressive multifocal leukoencephalopathy (PML). JCPyV is a human-only pathogen. Using the mouse polyomavirus (MuPyV) encephalitis model, we demonstrate that CD4 T cells regulate development of functional antiviral brain-resident CD8 T cells (bTRM) and renders their maintenance refractory to systemic CD8 T cell depletion. Acquired CD4 T cell deficiency, modeled by delaying systemic CD4 T cell depletion until MuPyV-specific CD8 T cells have infiltrated the brain, impacted the stability of CD8 bTRM, impaired their effector response to reinfection, and rendered their maintenance dependent on circulating CD8 T cells. This dependence of CD8 bTRM differentiation on CD4 T cells was found to extend to encephalitis caused by vesicular stomatitis virus. Together, these findings reveal an intimate association between CD4 T cells and homeostasis of functional bTRM to CNS viral infection. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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