In:
Cell and Tissue Research, Springer Science and Business Media LLC, Vol. 385, No. 2 ( 2021-08), p. 323-333
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0302-766X
,
1432-0878
DOI:
10.1007/s00441-021-03466-z
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2021
detail.hit.zdb_id:
1458496-7
SSG:
12
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