Arf6 and Rab22 mediate T cell conjugate formation by regulating clathrin-independent endosomal membrane trafficking
AffiliationUniv Arizona, Dept Cellular & Mol Med
MetadataShow full item record
PublisherCOMPANY OF BIOLOGISTS LTD
CitationArf6 and Rab22 mediate T cell conjugate formation by regulating clathrin-independent endosomal membrane trafficking 2017, 130 (14):2405 Journal of Cell Science
JournalJournal of Cell Science
Rights© 2017 The Author(s). Published by The Company of Biologists Ltd.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at email@example.com.
AbstractEndosomal trafficking can influence the composition of the plasma membrane and the ability of cells to polarize their membranes. Here, we examined whether trafficking through clathrin-independent endocytosis (CIE) affects the ability of T cells to form a cell-cell conjugate with antigen-presenting cells (APCs). We show that CIE occurs in both the Jurkat T cell line and primary human T cells. In Jurkat cells, the activities of two guanine nucleotide binding proteins, Arf6 and Rab22 (also known as Rab22a), influence CIE and conjugate formation. Expression of the constitutively active form of Arf6, Arf6Q67L, inhibits CIE and conjugate formation, and results in the accumulation of vacuoles containing lymphocyte function-associated antigen 1 (LFA-1) and CD4, molecules important for T cell interaction with the APC. Moreover, expression of the GTP-binding defective mutant of Rab22, Rab22S19N, inhibits CIE and conjugate formation, suggesting that Rab22 function is required for these activities. Furthermore, Jurkat cells expressing Rab22S19N were impaired in spreading onto coverslips coated with T cell receptor-activating antibodies. These observations support a role for CIE, Arf6 and Rab22 in conjugate formation between T cells and APCs.
Note12 Month Embargo; Published Online: 15 July 2017
VersionFinal published version
SponsorsIntramural Research Program in the National Heart, Lung, and Blood Institute at the National Institutes of Health (NIH) [HL0006060]; NIH [RO1 DK084047]