Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells
Autor: | Steven F. Ziegler, Avery W. Brewer, Marika Sarfati, Heidi K. Jessup, Nicole Paquette, Michael R. Comeau, Suzanne Chartier, Guy Delespesse, Bo-Rin Park Yoon, Zoulfia Allakhverdi |
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Rok vydání: | 2007 |
Předmět: |
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Complementary Thymic stromal lymphopoietin medicine.medical_treatment Immunology Enzyme-Linked Immunosorbent Assay Inflammation Biology Polymerase Chain Reaction Proinflammatory cytokine Allergic inflammation 03 medical and health sciences 0302 clinical medicine Thymic Stromal Lymphopoietin Hypersensitivity medicine Humans Immunology and Allergy Mast Cells Receptors Cytokine 030304 developmental biology Analysis of Variance 0303 health sciences Innate immune system Brief Definitive Report Epithelial Cells Immunity Innate 3. Good health Interleukin 33 Cytokine Cytokines Brief Definitive Reports Tumor necrosis factor alpha medicine.symptom 030215 immunology |
Zdroj: | The Journal of Experimental Medicine |
ISSN: | 1540-9538 0022-1007 |
DOI: | 10.1084/jem.20062211 |
Popis: | Compelling evidence suggests that the epithelial cell–derived cytokine thymic stromal lymphopoietin (TSLP) may initiate asthma or atopic dermatitis through a dendritic cell–mediated T helper (Th)2 response. Here, we describe how TSLP might initiate and aggravate allergic inflammation in the absence of T lymphocytes and immunoglobulin E antibodies via the innate immune system. We show that TSLP, synergistically with interleukin 1 and tumor necrosis factor, stimulates the production of high levels of Th2 cytokines by human mast cells (MCs). We next report that TSLP is released by primary epithelial cells in response to certain microbial products, physical injury, or inflammatory cytokines. Direct epithelial cell–mediated, TSLP-dependent activation of MCs may play a central role in “intrinsic” forms of atopic diseases and explain the aggravating role of infection and scratching in these diseases. |
Databáze: | OpenAIRE |
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