T helper cell trafficking in autoimmune kidney diseases
Open Access
- 17 February 2021
- journal article
- review article
- Published by Springer Science and Business Media LLC in Cell and tissue research
- Vol. 385 (2), 281-292
- https://doi.org/10.1007/s00441-020-03403-6
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.Keywords
Funding Information
- Deutsche Forschungsgemeinschaft (SFB 1192, SFB 1192)
- Projekt DEAL
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