Journal
JOURNAL OF IMMUNOLOGY
Volume 166, Issue 8, Pages 5099-5107Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.166.8.5099
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Funding
- NCI NIH HHS [CA38355] Funding Source: Medline
- NIAID NIH HHS [AI46710, AI21487] Funding Source: Medline
- NIA NIH HHS [AG01743] Funding Source: Medline
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A feature of T-APC interaction is that, via either TCR or CD28, T cells can absorb molecules from APC on to the cell surface and then internalize these molecules. Here, using both normal and TCR-transgenic T cells, we investigated the mechanism of T cell absorption of molecules from APC and the role of the cytoskeleton. The results show that although activated T cells could absorb APC molecules in the form of cell fragments, uptake of molecules by resting T cells required direct T-APC interaction. Based on studies with latrunculin B, surface absorption of molecules by resting T cells was crucially dependent upon the actin cytoskeleton for both CD28- and TCR-mediated absorption. Significantly, however, TCR-mediated absorption became strongly resistant to latrunculin B when the concentration of MHC-bound peptide on APC was raised to a high level, implying that the actin cytoskeleton is only important for absorption when the density of receptor/ligand interaction is low. By contrast, in all situations tested, the actin cytoskeleton played a decisive role in controlling T cell internalization of ligands from the cell surface. The Journal of Immunology, 2001.
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