Abstract
CD1d-restricted T-cells are activated by glycolipids presented by the major histocompatibility complex class-Ib molecule CD1d, found on the surface of antigen-presenting cells (APC). This interaction between APC, most notably dendritic cells (DC), and CD1d-restricted T-cells is an important regulatory step in the initiation of adaptive immune responses. It is well known that DC play a crucial role in the induction of contact hypersensitivity (CHS), a frequently studied form of in vivo T-cell-mediated immunity. In this study, we show that CD1d-restricted T-cells are also necessary for CHS, because both wild-type mice treated systemically or topically with CD1d glycolipid antagonists and CD1d-restricted T-cell-null mice have markedly diminished CHS responses. Thus, pharmacologic antagonists of CD1d can be used as effective inhibitors of CHS, a prototype for a variety of delayed-type tissue hypersensitivity responses.
Original language | English |
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Pages (from-to) | 250-8 |
Number of pages | 9 |
Journal | Experimental Dermatology |
Volume | 14 |
Issue number | 4 |
DOIs | |
Publication status | Published - Apr 2005 |
Keywords
- Administration, Topical
- Animals
- Antigen Presentation
- Antigens, CD1
- Antigens, CD1d
- Cell Line
- Dendritic Cells
- Dermatitis
- Dermatitis, Contact
- Dose-Response Relationship, Drug
- Glycolipids
- Hypersensitivity
- Killer Cells, Natural
- Major Histocompatibility Complex
- Mice
- Mice, Inbred BALB C
- Mice, Inbred C57BL
- Mice, Transgenic
- Mutation
- Oxazolone
- Phosphatidylethanolamines
- Polyethylene Glycols
- Receptors, Antigen, T-Cell