Mast Cells Have a Pivotal Role in TNF-Independent Lymph Node Hypertrophy and the Mobilization of Langerhans Cells in Response to Bacterial Peptidoglycan
Autor: | Geoffrey Rowden, Dunia Jawdat, Jean S. Marshall |
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Rok vydání: | 2006 |
Předmět: |
Staphylococcus aureus
Cellular differentiation Immunology Peptidoglycan Biology Lymphocyte Activation Mice chemistry.chemical_compound Cell Movement medicine Animals Immunology and Allergy Lectins C-Type Receptors Histamine H2 Mast Cells Receptors Histamine H1 Lymph node Adaptor Proteins Signal Transducing Mice Knockout Tumor Necrosis Factor-alpha Cell Differentiation Complement C3 Hypertrophy Dendritic cell Mast cell Mice Mutant Strains Toll-Like Receptor 2 Cell biology Mice Inbred C57BL Toll-Like Receptor 4 TLR2 Mannose-Binding Lectins medicine.anatomical_structure chemistry Langerhans Cells Antigens Surface Myeloid Differentiation Factor 88 TLR4 Tumor necrosis factor alpha Lymph Nodes |
Zdroj: | The Journal of Immunology. 177:1755-1762 |
ISSN: | 1550-6606 0022-1767 |
DOI: | 10.4049/jimmunol.177.3.1755 |
Popis: | 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/Wv 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. |
Databáze: | OpenAIRE |
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