Academic Journal
Engagement of NKG2D on bystander memory CD8 T cells promotes increased immunopathology following Leishmania major infection.
| العنوان: | Engagement of NKG2D on bystander memory CD8 T cells promotes increased immunopathology following Leishmania major infection. |
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| المؤلفون: | Erika J Crosby, Michael H Goldschmidt, E John Wherry, Phillip Scott |
| المصدر: | PLoS Pathogens, Vol 10, Iss 2, p e1003970 (2014) |
| بيانات النشر: | Public Library of Science (PLoS) |
| سنة النشر: | 2014 |
| المجموعة: | Directory of Open Access Journals: DOAJ Articles |
| مصطلحات موضوعية: | Immunologic diseases. Allergy, RC581-607, Biology (General), QH301-705.5 |
| الوصف: | One of the hallmarks of adaptive immunity is the development of a long-term pathogen specific memory response. While persistent memory T cells certainly impact the immune response during a secondary challenge, their role in unrelated infections is less clear. To address this issue, we utilized lymphocytic choriomeningitis virus (LCMV) and Listeria monocytogenes immune mice to investigate whether bystander memory T cells influence Leishmania major infection. Despite similar parasite burdens, LCMV and Listeria immune mice exhibited a significant increase in leishmanial lesion size compared to mice infected with L. major alone. This increased lesion size was due to a severe inflammatory response, consisting not only of monocytes and neutrophils, but also significantly more CD8 T cells. Many of the CD8 T cells were LCMV specific and expressed gzmB and NKG2D, but unexpectedly expressed very little IFN-γ. Moreover, if CD8 T cells were depleted in LCMV immune mice prior to challenge with L. major, the increase in lesion size was lost. Strikingly, treating with NKG2D blocking antibodies abrogated the increased immunopathology observed in LCMV immune mice, showing that NKG2D engagement on LCMV specific memory CD8 T cells was required for the observed phenotype. These results indicate that bystander memory CD8 T cells can participate in an unrelated immune response and induce immunopathology through an NKG2D dependent mechanism without providing increased protection. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| تدمد: | 1553-7366 1553-7374 |
| Relation: | http://europepmc.org/articles/PMC3937277?pdf=render; https://doaj.org/toc/1553-7366; https://doaj.org/toc/1553-7374; https://doaj.org/article/4e19db0efd7040d1907843174b89d448 |
| DOI: | 10.1371/journal.ppat.1003970 |
| الاتاحة: | https://doi.org/10.1371/journal.ppat.1003970 https://doaj.org/article/4e19db0efd7040d1907843174b89d448 |
| رقم الانضمام: | edsbas.4B30D057 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 15537366 15537374 |
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| DOI: | 10.1371/journal.ppat.1003970 |