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Koch, Stefan
Publications (10 of 24) Show all publications
Martins, L. R., Bung, R. K., Koch, S., Richter, K., Schwarzmüller, L., Terhardt, D., . . . Scholl, C. (2018). Stk33 is required for spermatid differentiation and male fertility in mice. Developmental Biology, 433(1), 84-93
Open this publication in new window or tab >>Stk33 is required for spermatid differentiation and male fertility in mice
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2018 (English)In: Developmental Biology, ISSN 0012-1606, E-ISSN 1095-564X, Vol. 433, no 1, p. 84-93Article in journal (Refereed) In press
Abstract [en]

Abstract Spermiogenesis is the final phase during sperm cell development in which round spermatids undergo dramatic morphological changes to generate spermatozoa. Here we report that the serine/threonine kinase Stk33 is essential for the differentiation of round spermatids into functional sperm cells and male fertility. Constitutive Stk33 deletion in mice results in severely malformed and immotile spermatozoa that are particularly characterized by disordered structural tail elements. Stk33 expression first appears in primary spermatocytes, and targeted deletion of Stk33 in these cells recapitulates the defects observed in constitutive knockout mice, confirming a germ cell-intrinsic function. Stk33 protein resides in the cytoplasm and partially co-localizes with the caudal end of the manchette, a transient structure that guides tail elongation, in elongating spermatids, and loss of Stk33 leads to the appearance of a tight, straight and elongated manchette. Together, these results identify Stk33 as an essential regulator of spermatid differentiation and male fertility.

Keywords
Stk33, Kinase, Spermiogenesis, Spermatogenesis, Infertility, Manchette
National Category
Basic Medicine
Identifiers
urn:nbn:se:liu:diva-143444 (URN)10.1016/j.ydbio.2017.11.007 (DOI)
Available from: 2017-12-07 Created: 2017-12-07 Last updated: 2018-02-06
Kirsch, N., Chang, L.-S., Koch, S., Glinka, A., Dolde, C., Colozza, G., . . . Niehrs, C. (2017). Angiopoietin-like 4 Is a Wnt Signaling Antagonist that Promotes LRP6 Turnover. Developmental Cell, 43(1), 71-+
Open this publication in new window or tab >>Angiopoietin-like 4 Is a Wnt Signaling Antagonist that Promotes LRP6 Turnover
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2017 (English)In: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 43, no 1, p. 71-+Article in journal (Refereed) Published
Abstract [en]

Angiopoietin-like 4 (ANGPTL4) is a secreted signaling protein that is implicated in cardiovascular disease, metabolic disorder, and cancer. Outside of its role in lipid metabolism, ANGPTL4 signaling remains poorly understood. Here, we identify ANGPTL4 as a Wnt signaling antagonist that binds to syndecans and forms a ternary complex with the Wnt co-receptor Lipoprotein receptor-related protein 6 (LRP6). This protein complex is internalized via clathrin-mediated endocytosis and degraded in lysosomes, leading to attenuation ofWnt/b-catenin signaling. Angptl4 is expressed in the Spemann organizer of Xenopus embryos and acts as a Wnt antagonist to promote notochord formation and prevent muscle differentiation. This unexpected function ofANGPTL4 invites reinterpretation of its diverse physiological effects in light of Wnt signaling and may open therapeutic avenues for human disease.

Place, publisher, year, edition, pages
CELL PRESS, 2017
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:liu:diva-142148 (URN)10.1016/j.devcel.2017.09.011 (DOI)000412557400009 ()29017031 (PubMedID)
Note

Funding Agencies|DFG [SFB 873]; HHMI

Available from: 2017-10-23 Created: 2017-10-23 Last updated: 2018-02-06
Koch, S. (2017). Extrinsic control of Wnt signaling in the intestine. Differentiation, 97, 1-8
Open this publication in new window or tab >>Extrinsic control of Wnt signaling in the intestine
2017 (English)In: Differentiation, ISSN 0301-4681, E-ISSN 1432-0436, Vol. 97, p. 1-8Article, review/survey (Refereed) Published
Abstract [en]

The canonical Wnt/beta-catenin signaling pathway is a central regulator of development and tissue homeostasis. In the intestine, Wnt signaling is primarily known as the principal organizer of epithelial stem cell identity and proliferation. Within the last decade, numerous scientific breakthroughs have shed light on epithelial self-organization in the gut, and organoids are now routinely used to study stem cell biology and intestinal pathophysiology. The contribution of non-epithelial cells to Wnt signaling in the gut has received less attention. However, there is mounting evidence that stromal cells are a rich source of Wnt pathway activators and inhibitors, which can dynamically shape Wnt signaling to control epithelial proliferation and restitution. Elucidating the extent and mechanisms of paracrine Wnt signaling in the intestine has the potential to broaden our understanding of epithelial homeostasis, and may be of particular relevance for disorders such as inflammatory bowel diseases and colitis-associated cancers.

Place, publisher, year, edition, pages
Elsevier, 2017
Keywords
Cell signaling, Intestinal epithelial cells, Colon, IBD, Colorectal cancer
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141655 (URN)10.1016/j.diff.2017.08.003 (DOI)000417863700001 ()28802143 (PubMedID)2-s2.0-85026869574 (Scopus ID)1432-0436 (Electronic) 0301-4681 (Linking) (ISBN)
Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Berger, B. S., Acebron, S. P., Herbst, J., Koch, S. & Niehrs, C. (2017). Parkinson's disease-associated receptor GPR37 is an ER chaperone for LRP6. EMBO Reports, 18(5), 712-725
Open this publication in new window or tab >>Parkinson's disease-associated receptor GPR37 is an ER chaperone for LRP6
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2017 (English)In: EMBO Reports, ISSN 1469-221X, E-ISSN 1469-3178, Vol. 18, no 5, p. 712-725Article in journal (Refereed) Published
Abstract [en]

Wnt/beta-catenin signaling plays a key role in embryonic development, stem cell biology, and neurogenesis. However, the mechanisms of Wnt signal transmission, notably how the receptors are regulated, remain incompletely understood. Here we describe that the Parkinson's disease-associated receptor GPR37 functions in the maturation of the N-terminal bulky beta-propellers of the Wnt co-receptor LRP6. GPR37 is required for Wnt/beta-catenin signaling and protects LRP6 from ER-associated degradation via CHIP (carboxyl terminus of Hsc70-interacting protein) and the ATPase VCP GPR37 is highly expressed in neural progenitor cells (NPCs) where it is required for Wnt-dependent neurogenesis. We conclude that GPR37 is crucial for cellular protein quality control during Wnt signaling.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2017
Keywords
ER-associated degradation; GPR37; LRP6; PAEL-R; Wnt signaling
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141651 (URN)10.15252/embr.201643585 (DOI)000400446100008 ()28341812 (PubMedID)2-s2.0-85017187389 (Scopus ID)1469-3178 (Electronic) 1469-221X (Linking) (ISBN)
Note

Berger, Birgit S Acebron, Sergio P Herbst, Jessica Koch, Stefan Niehrs, Christof eng England 2017/03/28 06:00 EMBO Rep. 2017 May;18(5):712-725. doi: 10.15252/embr.201643585. Epub 2017 Mar 24.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Koch, S., Acebron, S. P., Herbst, J., Hatiboglu, G. & Niehrs, C. (2015). Post-transcriptional Wnt Signaling Governs Epididymal Sperm Maturation. Cell, 163(5), 1225-1236
Open this publication in new window or tab >>Post-transcriptional Wnt Signaling Governs Epididymal Sperm Maturation
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2015 (English)In: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 163, no 5, p. 1225-1236Article in journal (Refereed) Published
Abstract [en]

The canonical Wnt signaling pathway is of paramount importance in development and disease. An emergent question is whether the upstream cascade of the canonical Wnt pathway has physiologically relevant roles beyond beta-catenin-mediated transcription, which is difficult to study due to the pervasive role of this protein. Here, we show that transcriptionally silent spermatozoa respond to Wnt signals released from the epididymis and that mice mutant for the Wnt regulator Cyclin Y-like 1 are male sterile due to immotile and malformed spermatozoa. Post-transcriptional Wnt signaling impacts spermatozoa through GSK3 by (1) reducing global protein poly-ubiquitination to maintain protein homeostasis; (2) inhibiting septin 4 phosphorylation to establish a membrane diffusion barrier in the sperm tail; and (3) inhibiting protein phosphatase 1 to initiate sperm motility. The results indicate that Wnt signaling orchestrates a rich post-transcriptional sperm maturation program and invite revisiting transcription-independent Wnt signaling in somatic cells as well.

Place, publisher, year, edition, pages
Cambridge, United States: Cell Press, 2015
Keywords
Animals, Axin Protein/metabolism, Cyclins/metabolism, Epididymis/*metabolism, *Gene Expression Regulation, Glycogen Synthase Kinase 3/metabolism, Male, Mice, Phosphorylation, Protein Processing, Post-Translational, RNA Processing, Post-Transcriptional, Septins/metabolism, *Sperm Maturation, *Wnt Signaling Pathway
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141656 (URN)10.1016/j.cell.2015.10.029 (DOI)000366044700020 ()26590424 (PubMedID)2-s2.0-84947756267 (Scopus ID)1097-4172 (Electronic) 0092-8674 (Linking) (ISBN)
Note

Koch, Stefan Acebron, Sergio P Herbst, Jessica Hatiboglu, Gencay Niehrs, Christof eng Research Support, Non-U.S. Gov't 2015/11/23 06:00 Cell. 2015 Nov 19;163(5):1225-1236. doi: 10.1016/j.cell.2015.10.029.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Neumann, P.-A., Koch, S., Hilgarth, R. S., Perez-Chanona, E., Denning, P., Jobin, C. & Nusrat, A. (2014). Gut commensal bacteria and regional Wnt gene expression in the proximal versus distal colon. American Journal of Pathology, 184(3), 592-9
Open this publication in new window or tab >>Gut commensal bacteria and regional Wnt gene expression in the proximal versus distal colon
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2014 (English)In: American Journal of Pathology, ISSN 0002-9440, E-ISSN 1525-2191, Am J Pathol, Vol. 184, no 3, p. 592-9Article in journal (Refereed) Published
Abstract [en]

Regional expression of Wingless/Int (Wnt) genes plays a central role in regulating intestinal development and homeostasis. However, our knowledge of such regional Wnt proteins in the colon remains limited. To understand further the effect of Wnt signaling components in controlling intestinal epithelial homeostasis, we investigated whether the physiological heterogeneity of the proximal and distal colon can be explained by differential Wnt signaling. With the use of a Wnt signaling-specific PCR array, expression of 84 Wnt-mediated signal transduction genes was analyzed, and a differential signature of Wnt-related genes in the proximal versus distal murine colon was identified. Several Wnt agonists (Wnt5a, Wnt8b, and Wnt11), the Wnt receptor frizzled family receptor 3, and the Wnt inhibitory factor 1 were differentially expressed along the colon length. These Wnt signatures were associated with differential epithelial cell proliferation and migration in the proximal versus distal colon. Furthermore, reduced Wnt/beta-catenin activity and decreased Wnt5a and Wnt11 expression were observed in mice lacking commensal bacteria, an effect that was reversed by conventionalization of germ-free mice. Interestingly, myeloid differentiation primary response gene 88 knockout mice showed decreased Wnt5a levels, indicating a role for Toll-like receptor signaling in regulating Wnt5a expression. Our results suggest that the morphological and physiological heterogeneity within the colon is in part facilitated by the differential expression of Wnt signaling components and influenced by colonization with bacteria.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Animals, Bacteria/*metabolism, Cell Proliferation, Colon/anatomy & histology/metabolism/*microbiology, Gene Expression Regulation, Bacterial, Mice, Mice, Inbred C57BL, Mice, Knockout, Microbiota, *Signal Transduction, Specific Pathogen-Free Organisms, Wnt Proteins/genetics/*metabolism, Wnt-5a Protein
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141667 (URN)10.1016/j.ajpath.2013.11.029 (DOI)000332055500003 ()24418259 (PubMedID)2-s2.0-84894111787 (Scopus ID)1525-2191 (Electronic) 0002-9440 (Linking) (ISBN)
Note

Neumann, Philipp-Alexander Koch, Stefan Hilgarth, Roland S Perez-Chanona, Ernesto Denning, Patricia Jobin, Christian Nusrat, Asma eng R01 DK073338/DK/NIDDK NIH HHS/ R01HD059122/HD/NICHD NIH HHS/ R01 HD059122/HD/NICHD NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ DK059888/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2014/01/15 06:00 Am J Pathol. 2014 Mar;184(3):592-9. doi: 10.1016/j.ajpath.2013.11.029. Epub 2014 Jan 11.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Nava, P., Kamekura, R., Quiros, M., Medina-Contreras, O., Hamilton, R. W., Kolegraff, K. N., . . . Nusrat, A. (2014). IFN gamma-induced suppression of beta-catenin signaling: evidence for roles of Akt and 14.3.3 zeta. Molecular Biology of the Cell, 25(19), 2894-2904
Open this publication in new window or tab >>IFN gamma-induced suppression of beta-catenin signaling: evidence for roles of Akt and 14.3.3 zeta
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2014 (English)In: Molecular Biology of the Cell, ISSN 1059-1524, E-ISSN 1939-4586, Vol. 25, no 19, p. 2894-2904Article in journal (Refereed) Published
Abstract [en]

The proinflammatory cytokine interferon gamma (IFNgamma ) influences intestinal epithelial cell (IEC) homeostasis in a biphasic manner by acutely stimulating proliferation that is followed by sustained inhibition of proliferation despite continued mucosal injury. beta-Catenin activation has been classically associated with increased IEC proliferation. However, we observed that IFNgamma inhibits IEC proliferation despite sustained activation of Akt/beta-catenin signaling. Here we show that inhibition of Akt/beta-catenin-mediated cell proliferation by IFNgamma is associated with the formation of a protein complex containing phosphorylated beta-catenin 552 (pbeta-cat552) and 14.3.3zeta. Akt1 served as a bimodal switch that promotes or inhibits beta-catenin transactivation in response to IFNgamma stimulation. IFNgamma initially promotes beta-catenin transactivation through Akt-dependent C-terminal phosphorylation of beta-catenin to promote its association with 14.3.3zeta. Augmented beta-catenin transactivation leads to increased Akt1 protein levels, and active Akt1 accumulates in the nucleus, where it phosphorylates 14.3.3zeta to translocate 14.3.3zeta/beta-catenin from the nucleus, thereby inhibiting beta-catenin transactivation and IEC proliferation. These results outline a dual function of Akt1 that suppresses IEC proliferation during intestinal inflammation.

Place, publisher, year, edition, pages
Bethesda, United States: American Society for Cell Biology, 2014
Keywords
14-3-3 Proteins/*metabolism, Animals, CHO Cells, Cell Line, Cell Proliferation, Cricetulus, Enzyme Activation, Inflammation, Interferon-gamma/metabolism/*pharmacology, Intestinal Mucosa/*cytology, Mice, Mice, Inbred C57BL, Phosphorylation, Protein Binding, Proto-Oncogene Proteins c-akt/antagonists & inhibitors/*metabolism, Signal Transduction, beta Catenin/*antagonists & inhibitors
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141665 (URN)10.1091/mbc.E13-09-0512 (DOI)000343124100002 ()25079689 (PubMedID)2-s2.0-84929255585 (Scopus ID)1939-4586 (Electronic) 1059-1524 (Linking) (ISBN)
Note

Nava, Porfirio Kamekura, Ryuta Quiros, Miguel Medina-Contreras, Oscar Hamilton, Ross W Kolegraff, Keli N Koch, Stefan Candelario, Aurora Romo-Parra, Hector Laur, Oskar Hilgarth, Roland S Denning, Timothy L Parkos, Charles A Nusrat, Asma eng R01 DK079392/DK/NIDDK NIH HHS/ DK55679/DK/NIDDK NIH HHS/ R29 DK055679/DK/NIDDK NIH HHS/ R01 DK097256/DK/NIDDK NIH HHS/ DK72564/DK/NIDDK NIH HHS/ DK64399/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ DK53202/DK/NIDDK NIH HHS/ 1R01DK097256/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ DK59888/DK/NIDDK NIH HHS/ DK79392/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ DK61379/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2014/08/01 06:00 Mol Biol Cell. 2014 Oct 1;25(19):2894-904. doi: 10.1091/mbc.E13-09-0512. Epub 2014 Jul 30.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-03-06Bibliographically approved
Koch, S., Capaldo, C. T., Hilgarth, R. S., Fournier, B., Parkos, C. A. & Nusrat, A. (2013). Protein kinase CK2 is a critical regulator of epithelial homeostasis in chronic intestinal inflammation. Mucosal Immunology, 6(1), 136-145
Open this publication in new window or tab >>Protein kinase CK2 is a critical regulator of epithelial homeostasis in chronic intestinal inflammation
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2013 (English)In: Mucosal Immunology, ISSN 1933-0219, E-ISSN 1935-3456, Vol. 6, no 1, p. 136-145Article in journal (Refereed) Published
Abstract [en]

The molecular mechanisms that restore intestinal epithelial homeostasis during colitis are incompletely understood. Here, we report that during intestinal inflammation, multiple inflammatory cytokines promote the activity of a master regulator of cell proliferation and apoptosis, serine/threonine kinase CK2. Enhanced mucosal CK2 protein expression and activity were observed in animal models of chronic colitis, particularly within intestinal epithelial cells (IECs). The in vitro treatment of intestinal epithelial cell lines with cytokines resulted in increased CK2 expression and nuclear translocation of its catalytic alpha subunit. Similarly, nuclear translocation of CK2alpha was a prominent feature observed in colonic crypts from individuals with ulcerative colitis and Crohn's disease. Further in vitro studies revealed that CK2 activity promotes epithelial restitution, and protects normal IECs from cytokine-induced apoptosis. These observations identify CK2 as a key regulator of homeostatic properties of the intestinal epithelium that serves to promote wound healing, in part through inhibition of apoptosis under conditions of inflammation.

Place, publisher, year, edition, pages
Nature Publishing Group, 2013
Keywords
Animals, Apoptosis/genetics, Casein Kinase II/genetics/*metabolism, Caspases/metabolism, Cell Line, Cell Nucleus/metabolism, Cell Proliferation, Colitis/chemically induced/genetics/*immunology/*metabolism, Disease Models, Animal, Epithelial Cells/metabolism, Gene Expression Regulation, Homeostasis/*immunology, Humans, Intestinal Mucosa/*immunology/*metabolism, Mice, Protein Transport, Rats, Wound Healing, beta Catenin/metabolism
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141657 (URN)10.1038/mi.2012.57 (DOI)000312895500014 ()22763408 (PubMedID)2-s2.0-84870943584 (Scopus ID)1935-3456 (Electronic) 1933-0219 (Linking) (ISBN)
Note

Koch, S Capaldo, C T Hilgarth, R S Fournier, B Parkos, C A Nusrat, A eng R01 DK079392/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ DK059888/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2012/07/06 06:00 Mucosal Immunol. 2013 Jan;6(1):136-45. doi: 10.1038/mi.2012.57. Epub 2012 Jul 4.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Koch, S. (2013). The Epithelial Barrier. In: D'Amato M., Rioux J. (Ed.), Molecular Genetics of Inflammatory Bowel Disease: (pp. 265-280). Springer Science+Business Media B.V.
Open this publication in new window or tab >>The Epithelial Barrier
2013 (English)In: Molecular Genetics of Inflammatory Bowel Disease / [ed] D'Amato M., Rioux J., Springer Science+Business Media B.V., 2013, p. 265-280Chapter in book (Refereed)
Place, publisher, year, edition, pages
Springer Science+Business Media B.V., 2013
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141991 (URN)10.1007/978-1-4614-8256-7_13 (DOI)9781461482567 (ISBN)
Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
Khounlotham, M., Kim, W., Peatman, E., Nava, P., Medina-Contreras, O., Addis, C., . . . Parkos, C. A. (2012). Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis. Immunity, 37(3), 563-573
Open this publication in new window or tab >>Compromised intestinal epithelial barrier induces adaptive immune compensation that protects from colitis
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2012 (English)In: Immunity, ISSN 1074-7613, E-ISSN 1097-4180, Vol. 37, no 3, p. 563-573Article in journal (Refereed) Published
Abstract [en]

Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epithelial permeability, bacterial translocation, and elevated colonic lymphocyte numbers, yet do not develop colitis. To investigate the contribution of adaptive immune compensation in response to increased intestinal epithelial permeability, we examined the susceptibility of F11r(-/-)Rag1(-/-) mice to acute colitis. Although negligible contributions of adaptive immunity in F11r(+/+)Rag1(-/-) mice were observed, F11r(-/-)Rag1(-/-) mice exhibited increased microflora-dependent colitis. Elimination of T cell subsets and cytokine analyses revealed a protective role for TGF-beta-producing CD4(+) T cells in F11r(-/-) mice. Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that was dependent upon CD4(+) T cells and TGF-beta. Absence of IgA in F11r(+/+)Igha(-/-) mice did not affect disease, whereas F11r(-/-)Igha(-/-) mice displayed markedly increased susceptibility to acute injury-induced colitis. These data establish a role for adaptive immune-mediated protection from acute colitis under conditions of intestinal epithelial barrier compromise.

Place, publisher, year, edition, pages
Cambridge, United States: Cell Press, 2012
Keywords
Adaptive Immunity/genetics/*immunology, Animals, Bacterial Translocation/genetics/immunology, CD4-Positive T-Lymphocytes/immunology/metabolism, Cell Adhesion Molecules/genetics/immunology, Colitis/chemically induced/genetics/*immunology, Dextran Sulfate, Epithelium/immunology/metabolism, Female, Flow Cytometry, Gene Expression, Homeodomain Proteins/genetics/immunology, Immunoglobulin A/genetics/immunology, Intestinal Mucosa/*immunology/metabolism/microbiology, Intestines/*immunology/metabolism/microbiology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Permeability, Receptors, Cell Surface/genetics/immunology, Reverse Transcriptase Polymerase Chain Reaction, Transforming Growth Factor beta/genetics/immunology/metabolism
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-141654 (URN)10.1016/j.immuni.2012.06.017 (DOI)000309199000019 ()22981539 (PubMedID)2-s2.0-84866523733 (Scopus ID)1097-4180 (Electronic) 1074-7613 (Linking) (ISBN)
Note

Khounlotham, Manirath Kim, Wooki Peatman, Eric Nava, Porfirio Medina-Contreras, Oscar Addis, Caroline Koch, Stefan Fournier, Benedicte Nusrat, Asma Denning, Timothy L Parkos, Charles A eng R29 DK055679/DK/NIDDK NIH HHS/ K99 AA017870/AA/NIAAA NIH HHS/ DK72564/DK/NIDDK NIH HHS/ DK061379/DK/NIDDK NIH HHS/ DK 064399/DK/NIDDK NIH HHS/ R01 DK072564/DK/NIDDK NIH HHS/ R24 DK064399/DK/NIDDK NIH HHS/ AA017870/AA/NIAAA NIH HHS/ DK59888/DK/NIDDK NIH HHS/ DK055679/DK/NIDDK NIH HHS/ R01 DK055679/DK/NIDDK NIH HHS/ R00 AA017870/AA/NIAAA NIH HHS/ R01 DK061379/DK/NIDDK NIH HHS/ R01 DK059888/DK/NIDDK NIH HHS/ R21 AI083554/AI/NIAID NIH HHS/ AI083554/AI/NIAID NIH HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't 2012/09/18 06:00 Immunity. 2012 Sep 21;37(3):563-73. doi: 10.1016/j.immuni.2012.06.017. Epub 2012 Sep 13.

Available from: 2017-10-16 Created: 2017-10-16 Last updated: 2018-01-13Bibliographically approved
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