Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Meredith Steeves"'
Publikováno v:
The Journal of Immunology. 189:669-678
IL-10 is a critical anti-inflammatory cytokine, the deficiency of which leads to spontaneous autoimmunity. However, therapeutically administered or ectopically expressed IL-10 can either suppress or promote disease. Distinct lineage-specific activiti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6f43f170e005e6984484c1562ae6a457
https://doi.org/10.4049/jimmunol.1200607
https://doi.org/10.4049/jimmunol.1200607
Autor:
Jing Ma, Xin Liu, Terrence L. Geiger, Phuong Nguyen, Wei Liu, Meredith Steeves, Cheng Cheng, John C. Obenauer
Summary The source, specificity, and plasticity of the forkhead box transcription factor 3 (Foxp3) + regulatory T (Treg) and conventional T (Tconv) cell populations active at sites of autoimmune pathology are not well characterized. To evaluate this,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::15b787fc2c815f6b4a0eb5c375f06150
https://europepmc.org/articles/PMC2878844/
https://europepmc.org/articles/PMC2878844/
After stimulation, T cells enter a transient refractory period, promoted by IL-2, during which they are resistant to re-stimulation. We previously demonstrated that these IL-2- and Ag-stimulated refractory T cells are able to suppress the Ag-induced
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::41adf2cdf17e168a8d9db1a0a09ccaba
https://europepmc.org/articles/PMC2559971/
https://europepmc.org/articles/PMC2559971/
Publikováno v:
The Journal of Immunology. 188:123.16-123.16
IL10 is a critical anti-inflammatory cytokine, deficiency of which leads to spontaneous autoimmunity. Yet therapeutically administered or ectopically expressed IL10 may either suppress or promote autoimmunity. Distinct lineage-specific activities may
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::408d3ae7c664ea0d1482dd63503e7822
https://doi.org/10.4049/jimmunol.188.supp.123.16
https://doi.org/10.4049/jimmunol.188.supp.123.16