Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.
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Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN. / Ostmann, Annett; Paust, Hans-Joachim; Panzer, Ulf; Wegscheid, Claudia; Kapffer, Sonja; Huber, Samuel; Flavell, Richard A; Erhardt, Annette; Tiegs, Gisa.
in: J AM SOC NEPHROL, Jahrgang 24, Nr. 6, 6, 2013, S. 930-942.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Regulatory T Cell-Derived IL-10 Ameliorates Crescentic GN.
AU - Ostmann, Annett
AU - Paust, Hans-Joachim
AU - Panzer, Ulf
AU - Wegscheid, Claudia
AU - Kapffer, Sonja
AU - Huber, Samuel
AU - Flavell, Richard A
AU - Erhardt, Annette
AU - Tiegs, Gisa
PY - 2013
Y1 - 2013
N2 - Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.
AB - Regulatory T cells (Tregs) exert their immunosuppressive activity through several immunoregulatory mechanisms, including the production of anti-inflammatory cytokines such as IL-10. Although several studies suggest a role for Tregs in modulating crescentic GN, the underlying mechanisms are not well understood. Here, using IL-10 reporter mice, we detected IL-10-producing Foxp3(+) T cells in the kidney, blood, and secondary lymphoid tissue in a mouse model of crescentic GN. Specific inactivation of Il10 in Foxp3(+) Tregs eliminated the ability of these cells to suppress renal and systemic production of IFNγ and IL-17; these IL-10-deficient Tregs lost their capacity to attenuate renal tissue injury. These data highlight the suppressive functions of Tregs in crescentic GN and suggest the importance of Treg-derived IL-10 in ameliorating disease severity and in modulating both the Th1 and most notably Th17 immune response.
KW - Animals
KW - B-Lymphocytes
KW - Blood Proteins
KW - Dendritic Cells
KW - Disease Models, Animal
KW - Forkhead Transcription Factors
KW - Glomerulonephritis
KW - Interleukin-10
KW - Kidney
KW - Macrophages
KW - Mice
KW - Mice, Inbred C57BL
KW - Mice, Knockout
KW - RNA, Messenger
KW - Severity of Illness Index
KW - Sheep
KW - Spleen
KW - T-Lymphocytes, Regulatory
KW - Th1 Cells
KW - Th17 Cells
U2 - 10.1681/ASN.2012070684
DO - 10.1681/ASN.2012070684
M3 - SCORING: Journal article
C2 - 23641052
VL - 24
SP - 930
EP - 942
JO - J AM SOC NEPHROL
JF - J AM SOC NEPHROL
SN - 1046-6673
IS - 6
M1 - 6
ER -