T helper cell trafficking in autoimmune kidney diseases.
Cell Tissue Res
; 385(2): 281-292, 2021 Aug.
Article
in En
| MEDLINE
| ID: mdl-33598825
ABSTRACT
CD4+ T cells are key drivers of autoimmune diseases, including crescentic GN. Many effector mechanisms employed by T cells to mediate renal damage and repair, such as local cytokine production, depend on their presence at the site of inflammation. Therefore, the mechanisms regulating the renal CD4+ T cell infiltrate are of central importance. From a conceptual point of view, there are four distinct factors that can regulate the abundance of T cells in the kidney (1) T cell infiltration, (2) T cell proliferation, (3) T cell death and (4) T cell retention/egress. While a substantial amount of data on the recruitment of T cells to the kidneys in crescentic GN have accumulated over the last decade, the roles of T cell proliferation and death in the kidney in crescentic GN is less well characterized. However, the findings from the data available so far do not indicate a major role of these processes. More importantly, the molecular mechanisms underlying both egress and retention of T cells from/in peripheral tissues, such as the kidney, are unknown. Here, we review the current knowledge of mechanisms and functions of T cell migration in renal autoimmune diseases with a special focus on chemokines and their receptors.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Autoimmune Diseases
/
T-Lymphocytes, Helper-Inducer
/
Kidney
/
Kidney Diseases
Limits:
Animals
/
Humans
Language:
En
Journal:
Cell Tissue Res
Year:
2021
Type:
Article
Affiliation country:
Germany