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Published on: April 18, 2016
Tetraspanins CD37 and CD151 differentially regulate Ag presentation and T-cell co-stimulation by DC
Kuo-Ching Sheng1, Annemiek B van Spriel, Kate H Gartlan
1The Burnet Institute of Medical Research and Public Health, A&RMC, Heidelberg, Australia.
Insights
Dendritic cells (DCs) lacking tetraspanins CD37 or CD151 surprisingly enhance T-cell activation. These findings reveal distinct roles for CD37 and CD151 in regulating T-cell responses via peptide-MHC presentation and co-stimulation.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Dendritic cells (DCs) initiate T-cell responses by presenting peptide-MHC complexes.
- Tetraspanins are hypothesized to promote T-cell activation by facilitating MHC multimerization.
Purpose of the Study:
- To investigate the role of tetraspanins CD37 and CD151 in DC-mediated T-cell activation.
- To determine if CD37 and CD151 are essential for MHC multimerization and T-cell receptor cross-linking.
Main Methods:
- Generated and analyzed DCs deficient in CD37 or CD151 expression.
- Assessed T-cell activation in response to peptide-MHC presentation by these DCs.
- Investigated the distinct mechanisms of CD37 and CD151 in regulating T-cell responses.
Main Results:
- DCs lacking CD37 or CD151 showed no developmental or maturation defects.
- These CD37- or CD151-deficient DCs were hyper-stimulatory to T cells.
- CD151 regulates T-cell co-stimulation, while CD37 regulates peptide/MHC presentation.
Conclusions:
- Tetraspanins CD37 and CD151 play critical, distinct roles in regulating DC-mediated T-cell activation.
- The proposed model of tetraspanins solely promoting MHC multimerization may need revision.
- These findings offer new insights into the complex mechanisms governing immune responses.
Abstract:
A major question in immunology is how DC can display limited amounts of individual peptide-MHC complexes and still induce cross-linking of T-cell receptors to initiate cellular responses. One suggested mechanism is that MHC exists at the cell surface in high avidity multimers, and tetraspanin proteins, known to laterally associate with both MHC classes I and II, promote MHC multimerisation. To validate this theory, we tested the ability of DC deficient in either one of two typical tetraspanin molecules: CD37 or CD151 to present peptide to Ag-specific T cells. Surprisingly, although they exhibited no developmental or maturation defects, DC lacking either CD37 or CD151 expression were hyper-stimulatory to T cells. We demonstrate that CD37 and CD151 control DC-mediated T-cell activation by two different mechanisms: CD151 regulates co-stimulation whereas CD37 regulates peptide/MHC presentation. The implications of these results on the model suggesting that tetraspanins promote MHC multimerisation are discussed.
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