B Cell–Specific Loss of Lyn Kinase Leads to Autoimmunity

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 de...

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Published inThe Journal of immunology (1950) Vol. 192; no. 3; pp. 919 - 928
Main Authors Lamagna, Chrystelle, Hu, Yongmei, DeFranco, Anthony L, Lowell, Clifford A
Format Journal Article
LanguageEnglish
Published United States 01.02.2014
Subjects
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
src-Family Kinases - deficiency
src-Family Kinases - genetics
src-Family Kinases - immunology
T-Lymphocyte Subsets - immunology
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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 lynflox/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 lynflox/floxCd79a-cre mice with myd88flox/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.
AbstractList 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.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.
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.
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 f/f 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, and increased numbers of plasma and B1a cells, similar to the lyn −/− animals. Within 8 months of life, B cell-specific Lyn mutant mice develop high titers of IgG anti-sm/RNP 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 f/f Cd79a-cre mice with myd88 f/f 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.
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 lynflox/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 lynflox/floxCd79a-cre mice with myd88flox/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.
Author Lamagna, Chrystelle
DeFranco, Anthony L
Lowell, Clifford A
Hu, Yongmei
AuthorAffiliation Department of Laboratory Medicine, University of California, San Francisco, CA, 94143 USA
Department of Microbiology and Immunology, University of California, San Francisco, CA, 94143 USA
AuthorAffiliation_xml – name: Department of Microbiology and Immunology, University of California, San Francisco, CA, 94143 USA
– name: Department of Laboratory Medicine, University of California, San Francisco, CA, 94143 USA
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  givenname: Chrystelle
  surname: Lamagna
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  givenname: Yongmei
  surname: Hu
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  givenname: Anthony L
  surname: DeFranco
  fullname: DeFranco, Anthony L
– sequence: 4
  givenname: Clifford A
  surname: Lowell
  fullname: Lowell, Clifford A
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24376269$$D View this record in MEDLINE/PubMed
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Snippet 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...
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...
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StartPage 919
SubjectTerms 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
src-Family Kinases - deficiency
src-Family Kinases - genetics
src-Family Kinases - immunology
T-Lymphocyte Subsets - immunology
Title B Cell–Specific Loss of Lyn Kinase Leads to Autoimmunity
URI https://www.ncbi.nlm.nih.gov/pubmed/24376269
https://www.proquest.com/docview/1490900063
https://pubmed.ncbi.nlm.nih.gov/PMC3900234
Volume 192
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