Tissue-resident memory T cells in renal autoimmune diseases
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Tissue-resident memory T cells in renal autoimmune diseases. / Ginsberg, Pauline; Panzer, Ulf; Asada, Nariaki.
in: FRONT IMMUNOL, Jahrgang 14, 2023, S. 1111521.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › Kurzpublikation › Forschung › Begutachtung
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TY - JOUR
T1 - Tissue-resident memory T cells in renal autoimmune diseases
AU - Ginsberg, Pauline
AU - Panzer, Ulf
AU - Asada, Nariaki
N1 - Copyright © 2023 Ginsberg, Panzer and Asada.
PY - 2023
Y1 - 2023
N2 - The discovery of tissue-resident memory T cells (TRM cells) reinterpreted the potential of human tissue-specific immunity. Following T cell receptor (TCR) activation and clonal expansion, effector T cells migrate to peripheral tissues where they remain long-term and differentiate to TRM cells after antigen clearance. This allows for prompt immunological responses upon antigen re-encounter. In addition to their protective properties in acute infections, recent studies have revealed that TRM cells might lead to aggravation of autoimmune diseases, such as lupus nephritis (LN) and anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (GN). These diseases present as proliferative and crescentic glomerulonephritis (cGN), which is a life-threatening condition leading to end-stage renal disease (ESRD) if left untreated. A better understanding of renal TRM cells might lead to identifying new therapeutic targets for relapsing autoimmune diseases of the kidney. In this review, we summarize the current knowledge of renal TRM cells and discuss their potential pathophysiological roles in renal autoimmune diseases.
AB - The discovery of tissue-resident memory T cells (TRM cells) reinterpreted the potential of human tissue-specific immunity. Following T cell receptor (TCR) activation and clonal expansion, effector T cells migrate to peripheral tissues where they remain long-term and differentiate to TRM cells after antigen clearance. This allows for prompt immunological responses upon antigen re-encounter. In addition to their protective properties in acute infections, recent studies have revealed that TRM cells might lead to aggravation of autoimmune diseases, such as lupus nephritis (LN) and anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (GN). These diseases present as proliferative and crescentic glomerulonephritis (cGN), which is a life-threatening condition leading to end-stage renal disease (ESRD) if left untreated. A better understanding of renal TRM cells might lead to identifying new therapeutic targets for relapsing autoimmune diseases of the kidney. In this review, we summarize the current knowledge of renal TRM cells and discuss their potential pathophysiological roles in renal autoimmune diseases.
KW - Humans
KW - Memory T Cells
KW - Kidney
KW - Glomerulonephritis
KW - Lupus Nephritis
KW - Kidney Failure, Chronic/complications
KW - Antibodies, Antineutrophil Cytoplasmic
U2 - 10.3389/fimmu.2023.1111521
DO - 10.3389/fimmu.2023.1111521
M3 - Short publication
C2 - 36756116
VL - 14
SP - 1111521
JO - FRONT IMMUNOL
JF - FRONT IMMUNOL
SN - 1664-3224
ER -
