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Staphylococcal Enterotoxin B Binds and Regulates CD1d in Human Renal Proximal Tubule Epithelial Cells
Author(s) -
Miller StacyAnn,
Hammamieh Rasha,
Lin Yixin,
Shupp Jeffrey,
Jett Marti
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.745.1
Staphylococcal eneterotoxin B (SEB), a monovalent T cell mitogen and inducer of T suppressor cells. SEB forms complexes with the major histocompatibility complex class II and T‐cell receptor (TCR) in a manner that is quite different from the way the natural ligands bind to the same receptors. It is estimated that within 90 min. post‐exposure to SEB, a significant percent of the toxin is cleared to the renal proximal tubule epithelial cells (RPTEC). It was hypothesized that SEB binds to RPTECs using a mechanism that does not involve MHC‐II. CD1d is a non‐classical MHC class I homologous protein that is present in the plasma membrane lipid rafts and said to be involved in presenting the antigen to the NK cells. SEBs ability to bind RPTECs was confirmed by fluorescent microscopy, and an increase in CD1d mRNA expression was seen after one hour in cells exposed to SEB. Co‐localization studies using fluorescent microscopy showed that the two molecular were interacting. Quantitative IP assays confirmed this. We also showed that SEB directly binds to CD1d using dotReady immunoassays. This work provides strong evidence that SEB is binding a surface molecule not associated with MHC‐II on kidney cells.