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CD1a-, b-, and c-restricted TCRs recognize both self and foreign antigens
Michael S Vincent1, Xiaowei Xiong, Ethan P Grant
1Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham & Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. mvicent@amgen.com
Journal of Immunology (Baltimore, Md. : 1950)
|November 8, 2005
Summary
This study reveals that T cells restricted by CD1 molecules can recognize both self and microbial lipids. This dual reactivity in T cell receptors (TCRs) suggests a combined capacity for rapid inflammatory responses and sustained, memory-generating immune reactions.
Area of Science:
- Immunology
- T cell biology
- Lipid antigen presentation
Background:
- T cells restricted by CD1 molecules recognize lipid antigens.
- The ability of a single CD1-restricted T cell receptor (TCR) to recognize both self and foreign lipids remains largely unexplored.
Purpose of the Study:
- To investigate the dual reactivity of CD1-restricted T cells towards both endogenous and microbial lipids.
- To characterize the TCRs involved in recognizing self and foreign lipid antigens presented by CD1 molecules.
Main Methods:
- Isolation and characterization of CD1a-, CD1b-, and CD1c-restricted T cells from human donors.
- Assays to measure T cell-mediated cytolysis and Interferon-gamma (IFN-γ) secretion.
- Analysis of T cell receptor (TCR) diversity and specificity.
Main Results:
- Identified CD1-restricted T cells that respond to self-lipids presented by CD1 molecules on dendritic cells.
- Observed that microbial lipids are potent agonists for the same CD1-restricted T cells.
- Found diverse alpha-beta TCRs conferring specificity for both self-CD1 and foreign lipid antigens.
Conclusions:
- CD1-restricted T cells exhibit dual reactivity, recognizing both self and foreign lipid antigens.
- This dual specificity suggests a coexistence of rapid inflammatory responses and adaptive, memory-generating immune responses.
- The findings have implications for understanding immune surveillance and response to infection and autoimmune conditions.