T cell plasticity in renal autoimmune disease
Standard
T cell plasticity in renal autoimmune disease. / Soukou, Shiwa; Huber, Samuel; Krebs, Christian F.
In: CELL TISSUE RES, Vol. 385, No. 2, 08.2021, p. 323-333.Research output: SCORING: Contribution to journal › SCORING: Review article › Research
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - T cell plasticity in renal autoimmune disease
AU - Soukou, Shiwa
AU - Huber, Samuel
AU - Krebs, Christian F
PY - 2021/8
Y1 - 2021/8
N2 - The presence of immune cells is a morphological hallmark of rapidly progressive glomerulonephritis, a disease group that includes anti-glomerular basement membrane glomerulonephritis, lupus nephritis, and anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. The cellular infiltrates include cells from both the innate and the adaptive immune responses. The latter includes CD4+ and CD8+ T cells. In the past, CD4+ T cell subsets were viewed as terminally differentiated lineages with limited flexibility. However, it is now clear that Th17 cells can in fact have a high degree of plasticity and convert, for example, into pro-inflammatory Th1 cells or anti-inflammatory Tr1 cells. Interestingly, Th17 cells in experimental GN display limited spontaneous plasticity. Here we review the literature of CD4+ T cell plasticity focusing on immune-mediated kidney disease. We point out the key findings of the past decade, in particular that targeting pathogenic Th17 cells by anti-CD3 injection can be a tool to modulate the CD4+ T cell response. This anti-CD3 treatment can trigger a regulatory phenotype in Th17 cells and transdifferentiation of Th17 cells into immunosuppressive IL-10-expressing Tr1 cells (Tr1exTh17 cells). Thus, targeting Th17 cell plasticity could be envisaged as a new therapeutic approach in patients with glomerulonephritis.
AB - The presence of immune cells is a morphological hallmark of rapidly progressive glomerulonephritis, a disease group that includes anti-glomerular basement membrane glomerulonephritis, lupus nephritis, and anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. The cellular infiltrates include cells from both the innate and the adaptive immune responses. The latter includes CD4+ and CD8+ T cells. In the past, CD4+ T cell subsets were viewed as terminally differentiated lineages with limited flexibility. However, it is now clear that Th17 cells can in fact have a high degree of plasticity and convert, for example, into pro-inflammatory Th1 cells or anti-inflammatory Tr1 cells. Interestingly, Th17 cells in experimental GN display limited spontaneous plasticity. Here we review the literature of CD4+ T cell plasticity focusing on immune-mediated kidney disease. We point out the key findings of the past decade, in particular that targeting pathogenic Th17 cells by anti-CD3 injection can be a tool to modulate the CD4+ T cell response. This anti-CD3 treatment can trigger a regulatory phenotype in Th17 cells and transdifferentiation of Th17 cells into immunosuppressive IL-10-expressing Tr1 cells (Tr1exTh17 cells). Thus, targeting Th17 cell plasticity could be envisaged as a new therapeutic approach in patients with glomerulonephritis.
U2 - 10.1007/s00441-021-03466-z
DO - 10.1007/s00441-021-03466-z
M3 - SCORING: Review article
C2 - 33937944
VL - 385
SP - 323
EP - 333
JO - CELL TISSUE RES
JF - CELL TISSUE RES
SN - 0302-766X
IS - 2
ER -