Reduced 2,4-dinitro-1-fluorobenzene-induced contact hypersensitivity response in IL-15 receptor??-deficient mice correlates with diminished CCL5/RANTES and CXCL10/IP-10 expression
| Autor: | Nan-Shih Liao, Lilan Hsu, Fang Liao, Jia-Perng Chen, Wan-Yu Mao, Min-Chi Ku, Szu-Liang Lai |
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| Rok vydání: | 2005 |
| Předmět: |
Male
medicine.medical_specialty Chemokine Immunology Gene Expression Enzyme-Linked Immunosorbent Assay Inflammation CD8-Positive T-Lymphocytes Biology Dermatitis Contact CCL5 Interferon-gamma Mice Internal medicine medicine Animals Immunology and Allergy CXCL10 Inducer Receptor Chemokine CCL5 Receptors Interleukin-15 Reverse Transcriptase Polymerase Chain Reaction Receptors Interleukin-2 hemic and immune systems Immunohistochemistry Chemokine CXCL10 Disease Models Animal Endocrinology Neutrophil Infiltration Interleukin 15 biology.protein Dinitrofluorobenzene Female Chemokines medicine.symptom Chemokines CXC CD8 |
| Zdroj: | European Journal of Immunology. 35:690-698 |
| ISSN: | 1521-4141 0014-2980 |
| Popis: | Using a model of 2,4-dinitro-1-fluorobenzene-induced contact hypersensitivity (CHS) we found that, as compared with wild-type mice, IL-15 receptor alpha chain (IL-15Ralpha)-deficient mice showed significantly less ear swelling. This decreased response was associated with diminished expression of CCL5/RANTES and CXCL10/IP-10, chemokines critical for effector cell recruitment, in the inflamed tissue. We determined that both the number of CD8(+) T cells infiltrating the affected skin and the production of CCL5/RANTES by antigen-stimulated CD8(+) T cells were decreased in IL-15Ralpha(-/-) mice. The lower levels of CXCL10/IP-10 suggested that the IL-15Ralpha(-/-) mice had reduced production of IFN-gamma, the primary inducer of CXCL10/IP-10, which was in fact the case. However, by contrast with CCL5/RANTES, the diminished levels of IFN-gamma were likely due to the decreased number of skin-infiltrating CD8(+) T cells, since IFN-gamma production by antigen-stimulated CD8(+) T cells was comparable between wild-type and IL-15Ralpha(-/-) mice. Our data suggest a positive, pro-inflammatory feedback loop involving CCL5/RANTES, IFN-gamma and CXCL10/IP-10 that underlies the CHS reaction and that is disrupted, likely primarily by a defect in CCL5/RANTES production, in mice lacking IL-15Ralpha, resulting in impaired leukocyte recruitment and inflammation. Moreover, it is particularly noteworthy that the defect in CCL5/RANTES expression in CD8(+) T cells is intrinsic to the absence of IL-15Ralpha, indicating that IL-15Ralpha is critical for CCL5/RANTES expression in CD8(+) T cells. |
| Databáze: | OpenAIRE |
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