The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
IL-12– and IL-23–modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition
Open accessAbstract
The interleukin (IL)-12p40 family of cytokines plays a critical role in the development of experimental autoimmune encephalomyelitis (EAE). However, the relative contributions of IL-12 and IL-23 to the pathogenic process remain to be elucidated. Here, we show that activation of uncommitted myelin-reactive T cells in the presence of either IL-12p70 or IL-23 confers encephalogenicity. Adoptive transfer of either IL-12p70– or IL-23–polarized T cells into naive syngeneic hosts resulted in an ascending paralysis that was clinically indistinguishable between the two groups. However, histological and reverse transcription–polymerase chain reaction analysis of central nervous system (CNS) tissues revealed distinct histopathological features and immune profiles. IL-12p70–driven disease was characterized by macrophage-rich infiltrates and prominent NOS2 up-regulation, whereas neutrophils and granulocyte–colony-stimulating factor (CSF) were prominent in IL-23–driven lesions. The monocyte-attracting chemokines CXCL9, 10, and 11 were preferentially expressed in the CNS of mice injected with IL-12p70–modulated T cells, whereas the neutrophil-attracting chemokines CXCL1 and CXCL2 were up-regulated in the CNS of mice given IL-23–modulated T cells. Treatment with anti–IL-17 or anti–granulocyte/macrophage-CSF inhibited EAE induced by transfer of IL-23–polarized, but not IL-12p70–polarized, cells. These findings indicate that autoimmunity can be mediated by distinct effector populations that use disparate immunological pathways to achieve a similar clinical outcome.
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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The spectrum of neuromyelitis optica
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Granulocyte Macrophage Colony-Stimulating Factor
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An Interleukin (IL)-10/IL-12 Immunoregulatory Circuit Controls Susceptibility to Autoimmune Disease
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Cited by
Kaser, A., Zeissig, S., & Blumberg, R. S. (2010) · Annual Review of Immunology · doi:10.1146/annurev-immunol-030409-101225 · Cited by 1,806
Filippi, M., Bar-Or, A., Piehl, F., Preziosa, P., Solari, A., Vukusic, S., & Rocca, M. A. (2018) · Nature Reviews Disease Primers · doi:10.1038/s41572-018-0041-4 · Cited by 1,562
Codarri, L., Gyülvészi, G., Tosevski, V., Hesske, L., Fontana, A., Magnenat, L., Suter, T., & Becher, B. (2011) · Nature Immunology · doi:10.1038/ni.2027 · Cited by 1,191
Reboldi, A., Coisne, C., Baumjohann, D., Benvenuto, F., Bottinelli, D., Lira, S., Uccelli, A., Lanzavecchia, A., Engelhardt, B., & Sallusto, F. (2009) · Nature Immunology · doi:10.1038/ni.1716 · Cited by 1,206
Hu, X., & Ivashkiv, L. B. (2009) · Immunity · doi:10.1016/j.immuni.2009.09.002 · Cited by 928
Metadata
- Authors
- Kroenke, M. A., Carlson, T. J., Andjelkovic, A. V., & Segal, B. M.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2008-06-23
- Volume
- 205
- Issue
- 7
- Pages
- 1535-1541
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2054235049
- Cited by
- 579
- References
- 29
- FWCI
- 48.03
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Kroenke, M. A., Carlson, T. J., Andjelkovic, A. V., & Segal, B. M. (2008). IL-12– and IL-23–modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20080159
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