Article
APL1, an altered peptide ligand derived from human heat-shock protein 60, increases the frequency of Tregs and its suppressive capacity against antigen responding effector CD4 + T cells from rheumatoid arthritis patients.
Cell stress & chaperones - 1 Jul 2016
Barberá Ariana, Lorenzo Noraylis, van Kooten Peter, van Roon Joel, de Jager Wilco, Prada Dinorah, Gómez Jorge, Padrón Gabriel, van Eden Willem, Broere Femke, Del Carmen Domínguez María
Abstract excerpt
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by a chronic relapsing-remitting joint inflammation. Perturbations in the balance between CD4 + T cells producing IL-17 and CD4 + CD25(high)FoxP3 + Tregs correlate with irreversible bone and cartilage destruction in RA. APL1 is an altered peptide ligand derived from a CD4+ T-cell epitope of human HSP60, an autoantigen expressed in the...
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