Journal
IMMUNITY
Volume 26, Issue 3, Pages 345-355Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2007.01.013
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Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NIAID NIH HHS [P01 AI071195-03, AI057966, AI034094, AI071195-01, P01 AI071195, R37 AI057966-05, R37 AI057966] Funding Source: Medline
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T cell activation is predicated on the interaction between the T cell receptor and peptide-major histocompatibility (pMHC) ligands. The factors that determine the stimulatory potency of a pMHC molecule remain unclear. We describe results showing that a peptide exhibiting many hallmarks of a weak agonist stimulates T cells to proliferate more than the wild-type agonist ligand. An in silico approach suggested that the inability to form the central supramolecular activation cluster (cSMAC) could underlie the increased proliferation. This conclusion was supported by experiments that showed that enhancing cSMAC formation reduced stimulatory capacity of the weak peptide. Our studies highlight the fact that a complex interplay of factors determines the quality of a T cell antigen.
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