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Mast Cells Have a Pivotal Role in TNF-Independent Lymph Node Hypertrophy and the Mobilization of Langerhans Cells in Response to Bacterial Peptidoglycan
Peptidoglycan (PGN) from Gram-positive bacteria, activates multiple immune effector cells. PGN-induced lymph node (LN) hypertrophy and dendritic cell mobilization in vivo were investigated following PGN injection into the skin. Both LN activation and the migration of Langerhans cells (LCs) to draini...
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| Published in: | Journal of Immunology 2006-08, Vol.177 (3), p.1755-1762 |
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| container_title | Journal of Immunology |
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| creator | Jawdat, Dunia M Rowden, Geoffrey Marshall, Jean S |
| description | Peptidoglycan (PGN) from Gram-positive bacteria, activates multiple immune effector cells. PGN-induced lymph node (LN) hypertrophy and dendritic cell mobilization in vivo were investigated following PGN injection into the skin. Both LN activation and the migration of Langerhans cells (LCs) to draining LNs were dependent on the presence of mast cells as demonstrated using mast cell deficient W/W(v) mice. However, these responses did not require TLR2, TLR4, or MYD88. TNF-deficient mice exhibited normal increases in LN cellularity but significantly reduced LC migration. In contrast, responses to IgE-mediated mast cell activation were highly TNF dependent. Complement component C3-deficient mice showed decreased LN hypertrophy and abrogated LC migration in response to PGN. These data demonstrate a critical role for mast cells and complement in LN responses to PGN and illustrate a novel TNF-independent mechanism whereby mast cells participate in the initiation of immunity. |
| doi_str_mv | 10.4049/jimmunol.177.3.1755 |
| format | article |
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PGN-induced lymph node (LN) hypertrophy and dendritic cell mobilization in vivo were investigated following PGN injection into the skin. Both LN activation and the migration of Langerhans cells (LCs) to draining LNs were dependent on the presence of mast cells as demonstrated using mast cell deficient W/W(v) mice. However, these responses did not require TLR2, TLR4, or MYD88. TNF-deficient mice exhibited normal increases in LN cellularity but significantly reduced LC migration. In contrast, responses to IgE-mediated mast cell activation were highly TNF dependent. Complement component C3-deficient mice showed decreased LN hypertrophy and abrogated LC migration in response to PGN. These data demonstrate a critical role for mast cells and complement in LN responses to PGN and illustrate a novel TNF-independent mechanism whereby mast cells participate in the initiation of immunity.</description><subject>Adaptor Proteins, Signal Transducing - deficiency</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - physiology</subject><subject>Animals</subject><subject>Antigens, Surface - biosynthesis</subject><subject>Bacteria</subject><subject>Cell Differentiation - immunology</subject><subject>Cell Movement - genetics</subject><subject>Cell Movement - immunology</subject><subject>Complement C3 - physiology</subject><subject>Hypertrophy</subject><subject>Langerhans Cells - immunology</subject><subject>Langerhans Cells - metabolism</subject><subject>Langerhans Cells - microbiology</subject><subject>Langerhans Cells - pathology</subject><subject>Lectins, C-Type - biosynthesis</subject><subject>Lymph Nodes - immunology</subject><subject>Lymph Nodes - metabolism</subject><subject>Lymph Nodes - microbiology</subject><subject>Lymph Nodes - pathology</subject><subject>Lymphocyte Activation - genetics</subject><subject>Lymphocyte Activation - immunology</subject><subject>Mannose-Binding Lectins - biosynthesis</subject><subject>Mast Cells - immunology</subject><subject>Mast Cells - microbiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Mutant Strains</subject><subject>Myeloid Differentiation Factor 88</subject><subject>Peptidoglycan - immunology</subject><subject>Receptors, Histamine H1 - physiology</subject><subject>Receptors, Histamine H2 - physiology</subject><subject>Staphylococcus aureus - immunology</subject><subject>Toll-Like Receptor 2 - deficiency</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - physiology</subject><subject>Toll-Like Receptor 4 - deficiency</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - physiology</subject><subject>Tumor Necrosis Factor-alpha - deficiency</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkc1u1DAURi0EotPCEyAhr2CVwR7_JUsY0U6laamqsrYc52biKrFD7OkoPAmPi6sZBDs2927O990rHYTeUbLkhFefHt0w7H3ol1SpJctTiBdoQYUghZREvkQLQlargiqpztB5jI-EEElW_DU6o7LkFS_FAv26MTHhNfR9xBvzBNjgO_cUkunxfegBO48fbi-La9_ACHn4hLfzMHb4NjSAN_MIU5rC2M3Y-AanDvBNqF3vfprkgsehxVvjdzB1xsfTmVx5D3EMPgJOAX8xNsHk8sE7GJNrwq6frfFv0KvW9BHenvYF-n759WG9Kbbfrq7Xn7eF5Uqlom2MpaKxlpK6VaJVdUVNraCxJRf1qjWlsivWVrallvGKgKCkFZyIUsrSNIpdoA_H3nEKP_YQkx5ctPlR4yHso5alFIxJ_l-QVkzKirIMsiNopxDjBK0eJzeYadaU6Gdz-o85nc1ppp_N5dT7U_2-HqD5mzmpysDHI9C5XXdwE-g4mL7PONWHw-Gfqt9SNqbt</recordid><startdate>20060801</startdate><enddate>20060801</enddate><creator>Jawdat, Dunia M</creator><creator>Rowden, Geoffrey</creator><creator>Marshall, Jean S</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20060801</creationdate><title>Mast Cells Have a Pivotal Role in TNF-Independent Lymph Node Hypertrophy and the Mobilization of Langerhans Cells in Response to Bacterial Peptidoglycan</title><author>Jawdat, Dunia M ; Rowden, Geoffrey ; Marshall, Jean S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-fdac15dcc10bf75f7b91ab7edc845b2fa87c23f9cf1c3490e510f54058668ad73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adaptor Proteins, Signal Transducing - deficiency</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - physiology</topic><topic>Animals</topic><topic>Antigens, Surface - biosynthesis</topic><topic>Bacteria</topic><topic>Cell Differentiation - immunology</topic><topic>Cell Movement - genetics</topic><topic>Cell Movement - immunology</topic><topic>Complement C3 - physiology</topic><topic>Hypertrophy</topic><topic>Langerhans Cells - immunology</topic><topic>Langerhans Cells - metabolism</topic><topic>Langerhans Cells - microbiology</topic><topic>Langerhans Cells - pathology</topic><topic>Lectins, C-Type - biosynthesis</topic><topic>Lymph Nodes - immunology</topic><topic>Lymph Nodes - metabolism</topic><topic>Lymph Nodes - microbiology</topic><topic>Lymph Nodes - pathology</topic><topic>Lymphocyte Activation - genetics</topic><topic>Lymphocyte Activation - immunology</topic><topic>Mannose-Binding Lectins - biosynthesis</topic><topic>Mast Cells - immunology</topic><topic>Mast Cells - microbiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Mutant Strains</topic><topic>Myeloid Differentiation Factor 88</topic><topic>Peptidoglycan - immunology</topic><topic>Receptors, Histamine H1 - physiology</topic><topic>Receptors, Histamine H2 - physiology</topic><topic>Staphylococcus aureus - immunology</topic><topic>Toll-Like Receptor 2 - deficiency</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - physiology</topic><topic>Toll-Like Receptor 4 - deficiency</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - physiology</topic><topic>Tumor Necrosis Factor-alpha - deficiency</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jawdat, Dunia M</creatorcontrib><creatorcontrib>Rowden, Geoffrey</creatorcontrib><creatorcontrib>Marshall, Jean S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jawdat, Dunia M</au><au>Rowden, Geoffrey</au><au>Marshall, Jean S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mast Cells Have a Pivotal Role in TNF-Independent Lymph Node Hypertrophy and the Mobilization of Langerhans Cells in Response to Bacterial Peptidoglycan</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2006-08-01</date><risdate>2006</risdate><volume>177</volume><issue>3</issue><spage>1755</spage><epage>1762</epage><pages>1755-1762</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>Peptidoglycan (PGN) from Gram-positive bacteria, activates multiple immune effector cells. PGN-induced lymph node (LN) hypertrophy and dendritic cell mobilization in vivo were investigated following PGN injection into the skin. Both LN activation and the migration of Langerhans cells (LCs) to draining LNs were dependent on the presence of mast cells as demonstrated using mast cell deficient W/W(v) mice. However, these responses did not require TLR2, TLR4, or MYD88. TNF-deficient mice exhibited normal increases in LN cellularity but significantly reduced LC migration. In contrast, responses to IgE-mediated mast cell activation were highly TNF dependent. Complement component C3-deficient mice showed decreased LN hypertrophy and abrogated LC migration in response to PGN. 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| ispartof | Journal of Immunology, 2006-08, Vol.177 (3), p.1755-1762 |
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| subjects | Adaptor Proteins, Signal Transducing - deficiency Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - physiology Animals Antigens, Surface - biosynthesis Bacteria Cell Differentiation - immunology Cell Movement - genetics Cell Movement - immunology Complement C3 - physiology Hypertrophy Langerhans Cells - immunology Langerhans Cells - metabolism Langerhans Cells - microbiology Langerhans Cells - pathology Lectins, C-Type - biosynthesis Lymph Nodes - immunology Lymph Nodes - metabolism Lymph Nodes - microbiology Lymph Nodes - pathology Lymphocyte Activation - genetics Lymphocyte Activation - immunology Mannose-Binding Lectins - biosynthesis Mast Cells - immunology Mast Cells - microbiology Mice Mice, Inbred C57BL Mice, Knockout Mice, Mutant Strains Myeloid Differentiation Factor 88 Peptidoglycan - immunology Receptors, Histamine H1 - physiology Receptors, Histamine H2 - physiology Staphylococcus aureus - immunology Toll-Like Receptor 2 - deficiency Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - physiology Toll-Like Receptor 4 - deficiency Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - physiology Tumor Necrosis Factor-alpha - deficiency Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - physiology |
| title | Mast Cells Have a Pivotal Role in TNF-Independent Lymph Node Hypertrophy and the Mobilization of Langerhans Cells in Response to Bacterial Peptidoglycan |
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