pattismith
Senior Member
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@bread.
Low CD8 is found in subsets of patients in RA, Polymyalgia Rheumatica or Giant Cell Arteritis...
Some ME/CFS patients as well, so we should look into this and try to understand this phenomenon...
Pro-inflammatory and Anti-inflammatory T cells in Giant Cell Arteritis 2016
Ryu Watanabe, M.D., Ph.D.,1 Ebru Hosgur, B.S.,1 Hui Zhang, M.D., Ph.D.,1 Zhenke Wen, M.D., Ph.D.,1 Gerald Berry, M.D.,2 Jörg J. Goronzy, M.D., Ph.D.,1 and Cornelia M. Weyand, M.D., Ph.D.
1 Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA
2 Department of Pathology, Stanford University School of Medicine, Stanford, CA
Abstract
Giant cell arteritis is an autoimmune disease defined by explicit tissue tropism to the walls of medium and large arteries.
Pathognomic inflammatory lesions are granulomatous in nature, emphasizing the functional role of CD4 T cells and macrophages.
Evidence for a pathogenic role of antibodies and immune complexes is missing.
Analysis of T cell populations in giant cell arteritis, both in the tissue lesions and in the circulation, has supported a model of broad, polyclonal T cell activation, involving an array of functional T cell lineages.
The signature of T cell cytokines produced by vasculitic lesions is typically multifunctional, including IL-2, IFN-γ, IL-17, IL-21, and GM-CSF, supportive for a general defect in T cell regulation.
Recent data describing the lack of a lymph node-based population of anti-inflammatory T cells in giant cell arteritis patients offers a fresh look at the immunopathology of this vasculitis.
Due to defective CD8+NOX2+ regulatory T cells, giant cell arteritis patients appear unable to curtail clonal expansion within the CD4 T cell compartment, resulting in wide-spread CD4 T cell hyperimmunity.
Why unopposed expansion of committed CD4 effector T cells would lead to invasion of the walls of medium and large arteries needs to be explored in further investigations.
Low CD8 is found in subsets of patients in RA, Polymyalgia Rheumatica or Giant Cell Arteritis...
Some ME/CFS patients as well, so we should look into this and try to understand this phenomenon...
Pro-inflammatory and Anti-inflammatory T cells in Giant Cell Arteritis 2016
Ryu Watanabe, M.D., Ph.D.,1 Ebru Hosgur, B.S.,1 Hui Zhang, M.D., Ph.D.,1 Zhenke Wen, M.D., Ph.D.,1 Gerald Berry, M.D.,2 Jörg J. Goronzy, M.D., Ph.D.,1 and Cornelia M. Weyand, M.D., Ph.D.
1 Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA
2 Department of Pathology, Stanford University School of Medicine, Stanford, CA
Abstract
Giant cell arteritis is an autoimmune disease defined by explicit tissue tropism to the walls of medium and large arteries.
Pathognomic inflammatory lesions are granulomatous in nature, emphasizing the functional role of CD4 T cells and macrophages.
Evidence for a pathogenic role of antibodies and immune complexes is missing.
Analysis of T cell populations in giant cell arteritis, both in the tissue lesions and in the circulation, has supported a model of broad, polyclonal T cell activation, involving an array of functional T cell lineages.
The signature of T cell cytokines produced by vasculitic lesions is typically multifunctional, including IL-2, IFN-γ, IL-17, IL-21, and GM-CSF, supportive for a general defect in T cell regulation.
Recent data describing the lack of a lymph node-based population of anti-inflammatory T cells in giant cell arteritis patients offers a fresh look at the immunopathology of this vasculitis.
Due to defective CD8+NOX2+ regulatory T cells, giant cell arteritis patients appear unable to curtail clonal expansion within the CD4 T cell compartment, resulting in wide-spread CD4 T cell hyperimmunity.
Why unopposed expansion of committed CD4 effector T cells would lead to invasion of the walls of medium and large arteries needs to be explored in further investigations.