Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]

Publication Date:
2018-12-11
Publisher:
The American Association of Immunologists (AAI)
Print ISSN:
0022-1767
Electronic ISSN:
1550-6606
Topics:
Medicine
Published by:
http://www.aai.org/
_version_ 1836399101316431872
autor Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
beschreibung Inflammatory bowel disease is associated with extraintestinal diseases such as primary sclerosing cholangitis in the liver. Interestingly, it is known that an imbalance between Foxp3 + regulatory T cells (Treg) and Th17 cells is involved in inflammatory bowel disease and also in primary sclerosing cholangitis. To explain these associations, one hypothesis is that intestinal inflammation and barrier defects promote liver disease because of the influx of bacteria and inflammatory cells to the liver. However, whether and how this is linked to the Treg and Th17 cell imbalance is unclear. To address this, we used dextran sodium sulfate (DSS) and T cell transfer colitis mouse models. We analyzed the pathological conditions of the intestine and liver on histological, cellular, and molecular levels. We observed bacterial translocation and an influx of inflammatory cells, in particular Th17 cells, to the liver during colitis. In the DSS colitis model, in which Treg were concomitantly increased in the liver, we did not observe an overt pathological condition of the liver. In contrast, the T cell–mediated colitis model, in which Treg are not abundant, was associated with marked liver inflammation and a pathological condition. Of note, upon depletion of Treg in DEREG mice, DSS colitis promotes accumulation of Th17 cells and a pathological condition of the liver. Finally, we studied immune cell migration using KAEDE mice and found that some of these cells had migrated directly from the inflamed intestine into the liver. Overall, these data indicate that colitis can promote a pathological condition of the liver and highlight an important role of Treg in controlling colitis-associated liver inflammation.
citation_standardnr 6367470
datenlieferant ipn_articles
feed_id 333
feed_publisher The American Association of Immunologists (AAI)
feed_publisher_url http://www.aai.org/
insertion_date 2018-12-11
journaleissn 1550-6606
journalissn 0022-1767
publikationsjahr_anzeige 2018
publikationsjahr_facette 2018
publikationsjahr_intervall 7984:2015-2019
publikationsjahr_sort 2018
publisher The American Association of Immunologists (AAI)
quelle Journal of Immunology
relation http://www.jimmunol.org/cgi/content/short/201/12/3558?rss=1
search_space articles
shingle_author_1 Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
shingle_author_2 Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
shingle_author_3 Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
shingle_author_4 Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
shingle_catch_all_1 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
Inflammatory bowel disease is associated with extraintestinal diseases such as primary sclerosing cholangitis in the liver. Interestingly, it is known that an imbalance between Foxp3 + regulatory T cells (Treg) and Th17 cells is involved in inflammatory bowel disease and also in primary sclerosing cholangitis. To explain these associations, one hypothesis is that intestinal inflammation and barrier defects promote liver disease because of the influx of bacteria and inflammatory cells to the liver. However, whether and how this is linked to the Treg and Th17 cell imbalance is unclear. To address this, we used dextran sodium sulfate (DSS) and T cell transfer colitis mouse models. We analyzed the pathological conditions of the intestine and liver on histological, cellular, and molecular levels. We observed bacterial translocation and an influx of inflammatory cells, in particular Th17 cells, to the liver during colitis. In the DSS colitis model, in which Treg were concomitantly increased in the liver, we did not observe an overt pathological condition of the liver. In contrast, the T cell–mediated colitis model, in which Treg are not abundant, was associated with marked liver inflammation and a pathological condition. Of note, upon depletion of Treg in DEREG mice, DSS colitis promotes accumulation of Th17 cells and a pathological condition of the liver. Finally, we studied immune cell migration using KAEDE mice and found that some of these cells had migrated directly from the inflamed intestine into the liver. Overall, these data indicate that colitis can promote a pathological condition of the liver and highlight an important role of Treg in controlling colitis-associated liver inflammation.
Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
The American Association of Immunologists (AAI)
0022-1767
00221767
1550-6606
15506606
shingle_catch_all_2 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
Inflammatory bowel disease is associated with extraintestinal diseases such as primary sclerosing cholangitis in the liver. Interestingly, it is known that an imbalance between Foxp3 + regulatory T cells (Treg) and Th17 cells is involved in inflammatory bowel disease and also in primary sclerosing cholangitis. To explain these associations, one hypothesis is that intestinal inflammation and barrier defects promote liver disease because of the influx of bacteria and inflammatory cells to the liver. However, whether and how this is linked to the Treg and Th17 cell imbalance is unclear. To address this, we used dextran sodium sulfate (DSS) and T cell transfer colitis mouse models. We analyzed the pathological conditions of the intestine and liver on histological, cellular, and molecular levels. We observed bacterial translocation and an influx of inflammatory cells, in particular Th17 cells, to the liver during colitis. In the DSS colitis model, in which Treg were concomitantly increased in the liver, we did not observe an overt pathological condition of the liver. In contrast, the T cell–mediated colitis model, in which Treg are not abundant, was associated with marked liver inflammation and a pathological condition. Of note, upon depletion of Treg in DEREG mice, DSS colitis promotes accumulation of Th17 cells and a pathological condition of the liver. Finally, we studied immune cell migration using KAEDE mice and found that some of these cells had migrated directly from the inflamed intestine into the liver. Overall, these data indicate that colitis can promote a pathological condition of the liver and highlight an important role of Treg in controlling colitis-associated liver inflammation.
Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
The American Association of Immunologists (AAI)
0022-1767
00221767
1550-6606
15506606
shingle_catch_all_3 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
Inflammatory bowel disease is associated with extraintestinal diseases such as primary sclerosing cholangitis in the liver. Interestingly, it is known that an imbalance between Foxp3 + regulatory T cells (Treg) and Th17 cells is involved in inflammatory bowel disease and also in primary sclerosing cholangitis. To explain these associations, one hypothesis is that intestinal inflammation and barrier defects promote liver disease because of the influx of bacteria and inflammatory cells to the liver. However, whether and how this is linked to the Treg and Th17 cell imbalance is unclear. To address this, we used dextran sodium sulfate (DSS) and T cell transfer colitis mouse models. We analyzed the pathological conditions of the intestine and liver on histological, cellular, and molecular levels. We observed bacterial translocation and an influx of inflammatory cells, in particular Th17 cells, to the liver during colitis. In the DSS colitis model, in which Treg were concomitantly increased in the liver, we did not observe an overt pathological condition of the liver. In contrast, the T cell–mediated colitis model, in which Treg are not abundant, was associated with marked liver inflammation and a pathological condition. Of note, upon depletion of Treg in DEREG mice, DSS colitis promotes accumulation of Th17 cells and a pathological condition of the liver. Finally, we studied immune cell migration using KAEDE mice and found that some of these cells had migrated directly from the inflamed intestine into the liver. Overall, these data indicate that colitis can promote a pathological condition of the liver and highlight an important role of Treg in controlling colitis-associated liver inflammation.
Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
The American Association of Immunologists (AAI)
0022-1767
00221767
1550-6606
15506606
shingle_catch_all_4 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
Inflammatory bowel disease is associated with extraintestinal diseases such as primary sclerosing cholangitis in the liver. Interestingly, it is known that an imbalance between Foxp3 + regulatory T cells (Treg) and Th17 cells is involved in inflammatory bowel disease and also in primary sclerosing cholangitis. To explain these associations, one hypothesis is that intestinal inflammation and barrier defects promote liver disease because of the influx of bacteria and inflammatory cells to the liver. However, whether and how this is linked to the Treg and Th17 cell imbalance is unclear. To address this, we used dextran sodium sulfate (DSS) and T cell transfer colitis mouse models. We analyzed the pathological conditions of the intestine and liver on histological, cellular, and molecular levels. We observed bacterial translocation and an influx of inflammatory cells, in particular Th17 cells, to the liver during colitis. In the DSS colitis model, in which Treg were concomitantly increased in the liver, we did not observe an overt pathological condition of the liver. In contrast, the T cell–mediated colitis model, in which Treg are not abundant, was associated with marked liver inflammation and a pathological condition. Of note, upon depletion of Treg in DEREG mice, DSS colitis promotes accumulation of Th17 cells and a pathological condition of the liver. Finally, we studied immune cell migration using KAEDE mice and found that some of these cells had migrated directly from the inflamed intestine into the liver. Overall, these data indicate that colitis can promote a pathological condition of the liver and highlight an important role of Treg in controlling colitis-associated liver inflammation.
Mathies, F., Steffens, N., Kleinschmidt, D., Stuhlmann, F., Huber, F. J., Roy, U., Meyer, T., Luetgehetmann, M., von Petersdorff, M., Seiz, O., Herkel, J., Schramm, C., Flavell, R. A., Gagliani, N., Krebs, C., Panzer, U., Abdullah, Z., Strowig, T., Bedke, T., Huber, S.
The American Association of Immunologists (AAI)
0022-1767
00221767
1550-6606
15506606
shingle_title_1 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
shingle_title_2 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
shingle_title_3 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
shingle_title_4 Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
timestamp 2025-06-30T23:37:37.528Z
titel Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
titel_suche Colitis Promotes a Pathological Condition of the Liver in the Absence of Foxp3+ Regulatory T Cells [IMMUNE REGULATION]
topic WW-YZ
uid ipn_articles_6367470