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Kinetics of human leukocyte antigen receptor HLA-DR(+) monocytes and T lymphocytes during remission induction therapy in ANCA-associated vasculitis

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is characterized by small vessel inflammation and the presence of autoantibodies against cytoplasmic proteases, most often proteinase-3 and myeloperoxidase. Peripheral blood monocytes are an important source of local macrophage accumu...

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Detalles Bibliográficos
Autores principales: Tampe, Désirée, Hakroush, Samy, Biggemann, Lorenz, Winkler, Martin Sebastian, Tampe, Björn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9107415/
https://www.ncbi.nlm.nih.gov/pubmed/35445945
http://dx.doi.org/10.1007/s40620-022-01330-z
Descripción
Sumario:Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is characterized by small vessel inflammation and the presence of autoantibodies against cytoplasmic proteases, most often proteinase-3 and myeloperoxidase. Peripheral blood monocytes are an important source of local macrophage accumulation within parenchymal organs, as evidenced by their presence in early lesions in ANCA-associated glomerulonephritis. Major histocompatibility complex (MHC) II cell surface receptor human leukocyte antigen receptor (HLA-DR) allows antigen presentation to T cells and is crucial for the initiation of an immune response. We herein report HLA-DR abundance in AAV and the kinetics of HLA-DR(+) monocytes and T lymphocytes during remission induction therapy in AAV. Life-threatening AAV with pulmonary hemorrhage and renal involvement was associated with the presence of HLA-DR in a considerable population of peripheral blood monocytes and T lymphocytes, and relapsing disease manifested despite persistent B cell depletion after remission induction with rituximab. Moreover, remission induction in AAV with steroids, plasma exchange and intravenous cyclophosphamide, and improvement of clinical symptoms were associated with a decrease in HLA-DR(+) differing between monocytes and T lymphocytes. Particularly, persistent suppression of HLA-DR(+) monocytes was observed during remission induction, while an initial decrease in HLA-DR(+) T lymphocytes was followed by recovery of this population during the further course. Detailed insights into HLA-DR kinetics could pave the way towards an increased understanding of immunopathology and identify patients that could mostly benefit from distinct remission induction regimens.