T helper cell trafficking in autoimmune kidney diseases
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T helper cell trafficking in autoimmune kidney diseases. / Riedel, Jan-Hendrik; Turner, Jan-Eric; Panzer, Ulf.
in: CELL TISSUE RES, Jahrgang 385, Nr. 2, 08.2021, S. 281-292.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - T helper cell trafficking in autoimmune kidney diseases
AU - Riedel, Jan-Hendrik
AU - Turner, Jan-Eric
AU - Panzer, Ulf
PY - 2021/8
Y1 - 2021/8
N2 - 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.
AB - 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.
U2 - 10.1007/s00441-020-03403-6
DO - 10.1007/s00441-020-03403-6
M3 - SCORING: Review article
C2 - 33598825
VL - 385
SP - 281
EP - 292
JO - CELL TISSUE RES
JF - CELL TISSUE RES
SN - 0302-766X
IS - 2
ER -