The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Stimulation of T cell autoreactivity by anomalous expression of NKG2D and its MIC ligands in rheumatoid arthritis
Open accessAbstract
Effector T cell responses can be modulated by competing positive or negative signals transduced by natural killer (NK) cell receptors. This raises the possibility that dominant T cell stimulation might promote autoimmune reactions. In rheumatoid arthritis (RA), the severity of autoimmune and inflammatory joint disease correlates with large numbers of CD4 + CD28 – T cells, which are scarce in healthy individuals. For poorly defined reasons, these T cells are autoreactive, implying that they may contribute to disease manifestations. CD4 + CD28 – T cells in peripheral blood and synovial tissue of RA patients were found to express NKG2D, a costimulatory receptor that is absent on normal CD4 T cells. NKG2D was induced by tumor necrosis factor α and IL-15, which are abundant in inflamed synovia and RA patient sera. RA synoviocytes aberrantly expressed the stress-inducible MIC ligands of NKG2D, which stimulated autologous CD4 + CD28 – T cell cytokine and proliferative responses. Peripheral blood serum samples of RA patients contained substantial amounts of synoviocyte-derived soluble MICA, which failed to induce down-modulation of NKG2D because of the opposing activity of tumor necrosis factor α and IL-15. These results suggest that a profound dysregulation of NKG2D and its MIC ligands may cause autoreactive T cell stimulation, thus promoting the self-perpetuating pathology in RA and possibly other autoimmune diseases.
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Activation of NK Cells and T Cells by NKG2D, a Receptor for Stress-Inducible MICA
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Self-citationAn Activating Immunoreceptor Complex Formed by NKG2D and DAP10
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Self-citationBroad tumor-associated expression and recognition by tumor-derived γδ T cells of MICA and MICB
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Self-citationCostimulation of CD8αβ T cells by NKG2D via engagement by MIC induced on virus-infected cells
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Cited by
Lanier, L. L. (2005) · Annual Review of Immunology · doi:10.1146/annurev.immunol.23.021704.115526 · Cited by 2,769
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Self-citationNKG2D-deficient mice are defective in tumor surveillance in models of spontaneous malignancy
Guerra, N., Tan, Y. X., Joncker, N. T., Choy, A., Gallardo, F., Xiong, N., Knoblaugh, S., Cado, D., Greenberg, N. R., & Raulet, D. H. (2008) · Immunity · doi:10.1016/j.immuni.2008.02.016 · Cited by 850
Regulation of Ligands for the NKG2D Activating Receptor
Raulet, D. H., Gasser, S., Gowen, B. G., Deng, W., & Jung, H. (2013) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032712-095951 · Cited by 848
A Direct Role for NKG2D/MICA Interaction in Villous Atrophy during Celiac Disease
Hüe, S., Mention, J.-J., Monteiro, R. C., Zhang, S., Cellier, C., Schmitz, J., Verkarre, V., Fodil, N., Bahram, S., Cerf-Bensussan, N., et al. (2004) · Immunity · doi:10.1016/j.immuni.2004.06.018 · Cited by 759
Metadata
- Authors
- Groh, V., Brühl, A., El-Gabalawy, H., Nelson, J. L., & Spies, T.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2003-07-23
- Volume
- 100
- Issue
- 16
- Pages
- 9452-9457
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2060387930
- Cited by
- 506
- References
- 34
- FWCI
- 10.61
- Type
- journal article
- Language
- en
- Open access
- green
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