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Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis
Whole-exome sequencing reveals activating STAT1 mutations in some patients with autosomal dominant chronic mucocutaneous candidiasis disease.
CCR8+FOXp3+ Treg cells as master drivers of immune regulation
The pivotal role of CCR8+ Treg cells in restraining immunity is demonstrated and the potential clinical implications of this discovery are highlighted.
CXCL11-dependent induction of FOXP3-negative regulatory T cells suppresses autoimmune encephalomyelitis.
Administration of CXCL11-Ig during the first episode of relapsing EAE in SJL/J mice not only led to rapid remission, but also prevented subsequent relapse, suggesting that CxCL11 has the potential to restrain inflammatory autoimmunity.
Long-lasting protective immunity to experimental autoimmune encephalomyelitis following vaccination with naked DNA encoding C-C chemokines.
Modulation of EAE with C-C chemokine DNA vaccines is dependent on targeting chemokines that are highly transcribed at the site of inflammation at the onset of disease.
CXCL12 (SDF-1α) suppresses ongoing experimental autoimmune encephalomyelitis by selecting antigen-specific regulatory T cells
The results not only demonstrate, for the first time, that a chemokine functions as a regulatory mediator, but also suggest a novel way for treating multiple sclerosis and possibly other inflammatory autoimmune diseases.
Tr1 cell-dependent active tolerance blunts the pathogenic effects of determinant spreading.
Evidence is brought about showing that Tr1 cells play a pivotal role in the regulation of T cell tolerance during determinant spread and that soluble peptide therapy with the determinant to which the autoimmune response spreads amplifies a de novo regulatory mechanism aimed to reduce the pathological consequences of determinant spreading.
Targeting the Function of IFN-γ-Inducible Protein 10 Suppresses Ongoing Adjuvant Arthritis1
It is shown here that during the course of adjuvant-induced arthritis the immune system mounts a notable Ab titer against self-IP-10, which demonstrates the pivotal role of this chemokine in T cell polarization during experimentally induced arthritis and suggests a practical way to interfere in the regulation of disease to provide protective immunity.
CCR5+ Myeloid-Derived Suppressor Cells Are Enriched and Activated in Melanoma Lesions.
These findings validate the importance of the CCR5/CCR5 ligand axis not only for MDSC recruitment but also for further activation of their immunosuppressive functions in the tumor microenvironment, with potentially broad therapeutic implications, given existing clinically available inhibitors of this axis.
C-C chemokine-encoding DNA vaccines enhance breakdown of tolerance to their gene products and treat ongoing adjuvant arthritis.
Repeated administration of naked DNA vaccines encoding MCP-1, MIP-1 alpha, or RANTES inhibited the development and progression of AA, even when each vaccine was administered only after the onset of disease.
Plasmid DNA Encoding IFN-γ-Inducible Protein 10 Redirects Antigen-Specific T Cell Polarization and Suppresses Experimental Autoimmune Encephalomyelitis1
It is demonstrated that during activation this chemokine drives naive CD4+ T cells into Th1 polarization, demonstrating not only the pivotal role of a Chemokine in T cell polarization and function but also its potential implications for plasmid DNA gene therapy.