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Article: Recognition of Tumor Nidogen-1 by Neutrophil C-Type Lectin Receptors.

Sionov, Ronit Vogt / Lamagna, Chrystelle / Granot, Zvi

2022 Volume 10, Issue 4

Abstract: Neutrophil-mediated cytotoxicity toward tumor cells requires cell contact and is mediated by hydrogen peroxide. We have recently shown that Cathepsin G expressed on the neutrophil surface interacts with tumor RAGE, and this interaction facilitates ... ...

Abstract	Neutrophil-mediated cytotoxicity toward tumor cells requires cell contact and is mediated by hydrogen peroxide. We have recently shown that Cathepsin G expressed on the neutrophil surface interacts with tumor RAGE, and this interaction facilitates neutrophil cytotoxicity. Interruption of the Cathepsin G-RAGE interaction led to 50-80% reduction in cytotoxicity, suggesting that additional interactions are also involved. Here we show that blocking antibodies to the C-type lectin receptors (CLRs) Clec4e and Dectin-1, but not those to NKG2D, attenuated murine neutrophil cytotoxicity towards murine tumor cells, suggesting a contributing role for these CLRs in neutrophil recognition of tumor cells. We further observed that the CLRs interact with tumor Nidogen-1 and Hspg2, two sulfated glycoproteins of the basement membrane. Both Nidogen-1 and Hspg2 were found to be expressed on the tumor cell surface. The knockdown of Nidogen-1, but not that of Hspg2, led to reduced susceptibility of the tumor cells to neutrophil cytotoxicity. Altogether, this study suggests a role for CLR-Nidogen-1 interaction in the recognition of tumor cells by neutrophils, and this interaction facilitates neutrophil-mediated killing of the tumor cells.
Language	English
Publishing date	2022-04-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10040908
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Article ; Online: Eliminating chronic myeloid leukemia stem cells by IRAK1/4 inhibitors

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 13

Abstract: Leukemic stem cells (LSCs) in chronic myeloid leukemia are resistant to imatinib and therefore are a cause of relapse. The authors show that IRAK1/4-NF-κB-PD-L1 signaling is critical to mediate imatinib resistance in LSCs and that combining imatinib with ...

Abstract	Leukemic stem cells (LSCs) in chronic myeloid leukemia are resistant to imatinib and therefore are a cause of relapse. The authors show that IRAK1/4-NF-κB-PD-L1 signaling is critical to mediate imatinib resistance in LSCs and that combining imatinib with blocking this signalling pathway can eliminate LSCs.
Keywords	Science ; Q
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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Article ; Online: Eliminating chronic myeloid leukemia stem cells by IRAK1/4 inhibitors.

Nature communications

2022 Volume 13, Issue 1, Page(s) 271

Abstract: Leukemia stem cells (LSCs) in chronic myeloid leukemia (CML) are quiescent, insensitive to BCR-ABL1 tyrosine kinase inhibitors (TKIs) and responsible for CML relapse. Therefore, eradicating quiescent CML LSCs is a major goal in CML therapy. Here, using a ...

Abstract	Leukemia stem cells (LSCs) in chronic myeloid leukemia (CML) are quiescent, insensitive to BCR-ABL1 tyrosine kinase inhibitors (TKIs) and responsible for CML relapse. Therefore, eradicating quiescent CML LSCs is a major goal in CML therapy. Here, using a G
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Chronic Disease ; Drug Resistance, Neoplasm/drug effects ; Female ; Fusion Proteins, bcr-abl/metabolism ; Humans ; Imatinib Mesylate/pharmacology ; Immune Checkpoint Inhibitors/pharmacology ; Interleukin-1 Receptor-Associated Kinases/drug effects ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Leukemia, Myeloid/drug therapy ; Male ; Mice ; Middle Aged ; Neoplastic Stem Cells/metabolism ; Protein Kinase Inhibitors/pharmacology
Chemical Substances	Antineoplastic Agents ; Immune Checkpoint Inhibitors ; Protein Kinase Inhibitors ; Imatinib Mesylate (8A1O1M485B) ; Fusion Proteins, bcr-abl (EC 2.7.10.2) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Irak1 protein, mouse (EC 2.7.11.1) ; Irak4 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2022-01-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-27928-8
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Article: The bone marrow constitutes a reservoir of pericyte progenitors.

Lamagna, Chrystelle / Bergers, Gabriele

Journal of leukocyte biology

2006 Volume 80, Issue 4, Page(s) 677–681

Abstract: Adult bone marrow is a rich reservoir of hematopoietic and mesenchymal stem and progenitor cells. Mobilization and recruitment of bone marrow-derived cells to injured or ischemic tissue or tumors endorse the initiation and maintenance of angiogenic ... ...

Abstract	Adult bone marrow is a rich reservoir of hematopoietic and mesenchymal stem and progenitor cells. Mobilization and recruitment of bone marrow-derived cells to injured or ischemic tissue or tumors endorse the initiation and maintenance of angiogenic processes in the adult by incorporating endothelial progenitor cells (EPC) into the developing vasculature and by recruiting accessory hematopoietic cells. Recent data have now revealed that the origin of bone marrow-derived vascular cells is not restricted to endothelial cells but also includes pericytes--the perivascular support cells. Several laboratories have now reported the existence of pericyte progenitor cells, and these cells, like EPC, can be mobilized and recruited to the remodeling vasculature under ischemic conditions and in tumors. This review focuses on pericytes in vessel formation and on recent discoveries about their bone marrow origin in the adult.
MeSH term(s)	Animals ; Blood Vessels/cytology ; Blood Vessels/pathology ; Bone Marrow Cells/cytology ; Endothelial Cells/cytology ; Humans ; Models, Biological ; Neoplasms/blood supply ; Neoplasms/pathology ; Neoplasms/physiopathology ; Neovascularization, Pathologic/physiopathology ; Neovascularization, Physiologic ; Pericytes/cytology ; Stem Cells/cytology
Language	English
Publishing date	2006-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0506309
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Article ; Online: B cell-specific loss of Lyn kinase leads to autoimmunity.

Lamagna, Chrystelle / Hu, Yongmei / DeFranco, Anthony L / Lowell, Clifford A

Journal of immunology (Baltimore, Md. : 1950)

2013 Volume 192, Issue 3, Page(s) 919–928

Abstract: The Lyn tyrosine kinase regulates inhibitory signaling in B and myeloid cells: loss of Lyn results in a lupus-like autoimmune disease with hyperactive B cells and myeloproliferation. We have characterized the relative contribution of Lyn-regulated ... ...

Abstract	The Lyn tyrosine kinase regulates inhibitory signaling in B and myeloid cells: loss of Lyn results in a lupus-like autoimmune disease with hyperactive B cells and myeloproliferation. We have characterized the relative contribution of Lyn-regulated signaling pathways in B cells specifically to the development of autoimmunity by crossing the novel lyn(flox/flox) animals with mice carrying the Cre recombinase under the control of the Cd79a promoter, resulting in deletion of Lyn in B cells. The specific deletion of Lyn in B cells is sufficient for the development of immune complex-mediated glomerulonephritis. The B cell-specific Lyn-deficient mice have no defects in early bone marrow B cell development but have reduced numbers of mature B cells with poor germinal centers, as well as increased numbers of plasma and B1a cells, similar to the lyn(-/-) animals. Within 8 mo of life, B cell-specific Lyn mutant mice develop high titers of IgG anti-Smith Ag ribonucleoprotein and anti-dsDNA autoantibodies, which deposit in their kidneys, resulting in glomerulonephritis. B cell-specific Lyn mutant mice also develop myeloproliferation, similar to the lyn(-/-) animals. The additional deletion of MyD88 in B cells, achieved by crossing lyn(flox/flox)Cd79a-cre mice with myd88(flox/flox) animals, reversed the autoimmune phenotype observed in B cell-specific Lyn-deficient mice by blocking production of class-switched pathogenic IgG autoantibodies. Our results demonstrate that B cell-intrinsic Lyn-dependent signaling pathways regulate B cell homeostasis and activation, which in concert with B cell-specific MyD88 signaling pathways can drive the development of autoimmune disease.
MeSH term(s)	Animals ; Antibodies, Antinuclear/biosynthesis ; Antibodies, Antinuclear/genetics ; Antibodies, Antinuclear/immunology ; Antibody Specificity ; Autoimmunity/immunology ; B-Lymphocytes/enzymology ; B-Lymphocytes/immunology ; Calcium Signaling/immunology ; Cell Count ; Disease Models, Animal ; Germinal Center/immunology ; Germinal Center/pathology ; Homeostasis ; Immune Complex Diseases/immunology ; Immune Complex Diseases/pathology ; Immunoglobulin Class Switching ; Immunoglobulin G/biosynthesis ; Immunoglobulin G/immunology ; Immunoglobulin M/biosynthesis ; Immunoglobulin M/immunology ; Kidney/immunology ; Kidney/pathology ; Lupus Nephritis/enzymology ; Lupus Nephritis/etiology ; Lupus Nephritis/immunology ; Lymphocyte Activation ; Lymphopoiesis/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid Differentiation Factor 88/deficiency ; Myeloid Differentiation Factor 88/immunology ; Myeloproliferative Disorders/enzymology ; Myeloproliferative Disorders/genetics ; Myeloproliferative Disorders/immunology ; Organ Specificity ; Plasma Cells/immunology ; Spleen/immunology ; Spleen/pathology ; T-Lymphocyte Subsets/immunology ; src-Family Kinases/deficiency ; src-Family Kinases/genetics ; src-Family Kinases/immunology
Chemical Substances	Antibodies, Antinuclear ; Immunoglobulin G ; Immunoglobulin M ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2013-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1301979
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Article ; Online: Chapter 3. Bone marrow-derived vascular progenitors and proangiogenic monocytes in tumors.

Lu, Kan / Lamagna, Chrystelle / Bergers, Gabriele

Methods in enzymology

2008 Volume 445, Page(s) 53–82

Abstract: In tumors, new blood vessels develop not only from pre-existing vessels (angiogenesis), but can also be comprised of circulating vascular progenitor cells originating from the bone marrow (vasculogenesis). Besides endothelial progenitor cells (EPC) and ... ...

Abstract	In tumors, new blood vessels develop not only from pre-existing vessels (angiogenesis), but can also be comprised of circulating vascular progenitor cells originating from the bone marrow (vasculogenesis). Besides endothelial progenitor cells (EPC) and pericyte progenitor cells (PPCs) that are incorporated into the growing vasculature, other subpopulations of bone marrow-derived cells (BMDC) contribute indirectly to tumor neovascularization by providing growth factors, cytokines, and other key proangiogenic molecules. Here, we describe specific methods that allow for the identification and functional characterization of these distinct BMDC populations in tumors as exemplified in mouse models of pancreatic neuroendocrine tumors and glioblastomas.
MeSH term(s)	Animals ; Blood Vessels/cytology ; Blood Vessels/metabolism ; Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; Cell Differentiation ; Immunohistochemistry ; Monocytes/cytology ; Monocytes/metabolism ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Stem Cells/cytology ; Stem Cells/metabolism
Language	English
Publishing date	2008
Publishing country	United States
Document type	Journal Article
ISSN	1557-7988 ; 0076-6879
ISSN (online)	1557-7988
ISSN	0076-6879
DOI	10.1016/S0076-6879(08)03003-6
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Article ; Online: Hyperactivated MyD88 signaling in dendritic cells, through specific deletion of Lyn kinase, causes severe autoimmunity and inflammation.

Lamagna, Chrystelle / Scapini, Patrizia / van Ziffle, Jessica A / DeFranco, Anthony L / Lowell, Clifford A

Proceedings of the National Academy of Sciences of the United States of America

2013 Volume 110, Issue 35, Page(s) E3311–20

Abstract: Deletion of lyn, a Src-family tyrosine kinase expressed by B, myeloid, and dendritic cells (DCs), triggers lupus-like disease in mice, characterized by autoantibody production and renal immune complex deposition leading to chronic glomerulonephritis. B ... ...

Abstract	Deletion of lyn, a Src-family tyrosine kinase expressed by B, myeloid, and dendritic cells (DCs), triggers lupus-like disease in mice, characterized by autoantibody production and renal immune complex deposition leading to chronic glomerulonephritis. B cells from these mice are hyperactive to antigen-receptor stimulation owing to a loss of inhibitory signaling mediated by Lyn kinase. The hyperactive B-cell responses are thought to underlie the development of autoimmunity in this model. Lyn-deficient mice also manifest significant myeloexpansion. To test the contribution of different immune cell types to the lupus-like disease in this model, we generated a lyn(flox/flox) transgenic mouse strain. To our surprise, when we crossed these mice to Cd11c-cre animals, generating DC-specific deletion of Lyn, the animals developed spontaneous B- and T-cell activation and subsequent production of autoantibodies and severe nephritis. Remarkably, the DC-specific Lyn-deficient mice also developed severe tissue inflammatory disease, which was not present in the global lyn(-/-) strain. Lyn-deficient DCs were hyperactivated and hyperresponsive to Toll-like receptor agonists and IL-1β. To test whether dysregulation of these signaling pathways in DCs contributed to the inflammatory/autoimmune phenotype, we crossed the lyn(f/f) Cd11c-cre(+) mice to myd88(f/f) animals, generating double-mutant mice lacking both Lyn and the adaptor protein myeloid differentiation factor 88 (MyD88) in DCs, specifically. Deletion of MyD88 in DCs alone completely reversed the inflammatory autoimmunity in the DC-specific Lyn-mutant mice. Thus, we demonstrate that hyperactivation of MyD88-dependent signaling in DCs is sufficient to drive pathogenesis of lupus-like disease, illuminating the fact that dysregulation in innate immune cells alone can lead to autoimmunity.
MeSH term(s)	Animals ; Autoantibodies/biosynthesis ; Autoimmunity ; Dendritic Cells/enzymology ; Dendritic Cells/immunology ; Dendritic Cells/metabolism ; Inflammation/metabolism ; Lymphatic Diseases/genetics ; Lymphatic Diseases/metabolism ; Lymphocyte Activation ; Mice ; Mice, Knockout ; Myeloid Differentiation Factor 88/metabolism ; Signal Transduction ; Splenomegaly/genetics ; Splenomegaly/metabolism ; src-Family Kinases/genetics
Chemical Substances	Autoantibodies ; Myd88 protein, mouse ; Myeloid Differentiation Factor 88 ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2013-08-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1300617110
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Article: Dual role of macrophages in tumor growth and angiogenesis.

Lamagna, Chrystelle / Aurrand-Lions, Michel / Imhof, Beat A

Journal of leukocyte biology

2006 Volume 80, Issue 4, Page(s) 705–713

Abstract: During the neoplastic progression, macrophages as well as dendritic and NK cells are attracted into the tumor site and initiate the immune response against transformed cells. They activate and present tumor antigens to T cells, which are then activated ... ...

Abstract	During the neoplastic progression, macrophages as well as dendritic and NK cells are attracted into the tumor site and initiate the immune response against transformed cells. They activate and present tumor antigens to T cells, which are then activated to kill tumor cells. However, tumor cells are often capable of escaping the immune machinery. As the immune surveillance is not sufficient anymore, tumor-associated macrophages contribute to tumor progression. It is notable that tumor-associated macrophages promote the proliferation of tumor cells directly by secreting growth factors. They also participate in tumor progression by acting on endothelial cells and thus promoting the neovascularization of the tumor. Tumor-associated macrophages are indeed key protagonists during angiogenesis and promote each step of the angiogenesis cascade.
MeSH term(s)	Animals ; Humans ; Macrophages/immunology ; Macrophages/pathology ; Models, Biological ; Neoplasms/immunology ; Neoplasms/pathology ; Neovascularization, Pathologic/immunology ; Neovascularization, Pathologic/pathology
Language	English
Publishing date	2006-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.1105656
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Article ; Online: B cell-derived IL-10 suppresses inflammatory disease in Lyn-deficient mice.

Scapini, Patrizia / Lamagna, Chrystelle / Hu, Yongmei / Lee, Karim / Tang, Qizhi / DeFranco, Anthony L / Lowell, Clifford A

Proceedings of the National Academy of Sciences of the United States of America

2011 Volume 108, Issue 41, Page(s) E823–32

Abstract: Lyn kinase deficient mice represent a well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus erythematosus. We report that IL-10 plays a crucial immunosuppressive role in this model, modulating the ... ...

Abstract	Lyn kinase deficient mice represent a well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus erythematosus. We report that IL-10 plays a crucial immunosuppressive role in this model, modulating the inflammatory component of the disease caused by myeloid and T-cell activation. Double-mutant lyn(-/-)IL-10(-/-) mice manifested severe splenomegaly and lymphadenopathy, dramatically increased proinflammatory cytokine production, and severe tissue inflammation. Single-mutant lyn(-/-)mice showed expansion of IL-10-producing B cells. Interestingly, WT B cells adoptively transferred into lyn(-/-) mice showed increased differentiation into IL-10-producing B cells that assumed a similar phenotype to endogenous lyn(-/-) IL-10-producing B cells, suggesting that the inflammatory environment present in lyn(-/-) mice induces IL-10-producing B-cell differentiation. B cells, but not T or myeloid cells, were the critical source of IL-10 able to reduce inflammation and autoimmunity in double mutant lyn(-/-)IL-10(-/-) mice. IL-10 secretion by B cells was also crucial to sustain transcription factor Forkhead Box P3 (Foxp3) expression in regulatory T cells during disease development. These data reveal a dominant immunosuppressive function of B-cell-derived IL-10 in the Lyn-deficient model of autoimmunity, extending our current understanding of the role of IL-10 and IL-10-producing B cells in systemic lupus erythematosus.
MeSH term(s)	Animals ; B-Lymphocytes, Regulatory/enzymology ; B-Lymphocytes, Regulatory/immunology ; B-Lymphocytes, Regulatory/pathology ; Cell Differentiation ; Cytokines/biosynthesis ; Disease Models, Animal ; Humans ; Inflammation/immunology ; Inflammation/pathology ; Inflammation/prevention & control ; Inflammation Mediators/metabolism ; Interleukin-10/deficiency ; Interleukin-10/genetics ; Interleukin-10/physiology ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Lupus Erythematosus, Systemic/prevention & control ; Lymphatic Diseases/etiology ; Lymphatic Diseases/pathology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Myeloid Cells/immunology ; Splenomegaly/etiology ; Splenomegaly/pathology ; T-Lymphocytes/immunology ; src-Family Kinases/deficiency ; src-Family Kinases/genetics
Chemical Substances	Cytokines ; IL10 protein, mouse ; Inflammation Mediators ; Interleukin-10 (130068-27-8) ; lyn protein-tyrosine kinase (EC 2.7.10.2) ; src-Family Kinases (EC 2.7.10.2)
Language	English
Publishing date	2011-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1107913108
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Article: B cell-derived IL-10 suppresses inflammatory disease in Lyn-deficient mice

Scapini, Patrizia / Lamagna, Chrystelle / Hu, Yongmei / Lee, Karim / Tang, Qizhi / DeFranco, Anthony L / Lowell, Clifford A

Proceedings of the National Academy of Sciences of the United States of America. 2011 Oct. 11, v. 108, no. 41

2011

Abstract	Lyn kinase deficient mice represent a well established genetic model of autoimmune/autoinflammatory disease that resembles systemic lupus erythematosus. We report that IL-10 plays a crucial immunosuppressive role in this model, modulating the inflammatory component of the disease caused by myeloid and T-cell activation. Double-mutant lyn–/–IL-10–/– mice manifested severe splenomegaly and lymphadenopathy, dramatically increased proinflammatory cytokine production, and severe tissue inflammation. Single-mutant lyn–/–mice showed expansion of IL-10–producing B cells. Interestingly, WT B cells adoptively transferred into lyn–/– mice showed increased differentiation into IL-10–producing B cells that assumed a similar phenotype to endogenous lyn–/– IL-10–producing B cells, suggesting that the inflammatory environment present in lyn–/– mice induces IL-10–producing B-cell differentiation. B cells, but not T or myeloid cells, were the critical source of IL-10 able to reduce inflammation and autoimmunity in double mutant lyn–/–IL-10–/– mice. IL-10 secretion by B cells was also crucial to sustain transcription factor Forkhead Box P3 (Foxp3) expression in regulatory T cells during disease development. These data reveal a dominant immunosuppressive function of B-cell–derived IL-10 in the Lyn-deficient model of autoimmunity, extending our current understanding of the role of IL-10 and IL-10–producing B cells in systemic lupus erythematosus.
Keywords	T-lymphocytes ; autoimmunity ; inflammation ; interleukin-10 ; lupus erythematosus ; mice ; models ; mutants ; phenotype ; secretion ; splenomegaly ; transcription factors
Language	English
Dates of publication	2011-1011
Size	p. E823-E832.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
Database	NAL-Catalogue (AGRICOLA)

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