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pH-dependent interdomain tethers of CD1b regulate its antigen capture.

Miguel Relloso1, Tan-Yun Cheng, Jin S Im

  • 1Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Smith Building Room 514, 1 Jimmy Fund Way, Boston, MA 02115, USA.

Immunity
|June 10, 2008
PubMed
Summary

Changes in proton concentration within endosomes alter CD1b protein conformation, controlling lipid antigen loading. This pH-dependent mechanism regulates antigen capture by CD1b during endosomal recycling.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Structural Biology

Background:

  • CD1 proteins are crucial for lipid antigen presentation.
  • CD1 protein receptiveness to lipid antigen loading varies with cellular location.
  • Endosomal pH changes are hypothesized to influence CD1 protein function.

Purpose of the Study:

  • To investigate how pH-dependent changes in CD1b protein influence lipid antigen loading.
  • To identify specific residues and structural elements involved in pH-mediated regulation of CD1b.
  • To elucidate the mechanism by which CD1b controls antigen capture during endosomal recycling.

Main Methods:

  • Molecular dynamics simulations of the CD1b heavy chain.
  • Analysis of residue charge states and their pH-dependence.
  • Experimental disruption of identified tethers via acid pH treatment or mutation.
  • Assessing lipid association/dissociation and antigen presentation.

Main Results:

  • Molecular dynamics revealed flexible regions in the CD1b A' pocket.
  • pH-sensitive residues (D60, E62) tether rigid and flexible structural elements.
  • Disruption of these tethers increased lipid exchange and favored presentation of bulky lipid antigens.
  • Ionic tethers act as pH-sensitive molecular switches.

Conclusions:

  • Proton concentration in endosomes modulates CD1b conformation via ionic tethers.
  • This pH-dependent conformational change regulates the capture of lipid antigens.
  • The findings provide a mechanism for CD1b's role in adaptive immunity.