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Updated: Sep 2, 2026

Isolating Lymphocytes from the Mouse Small Intestinal Immune System
Published on: February 28, 2018
Glycosylphosphatidyl inositol-linked membrane protein expression by intestinal intraepithelial lymphocytes
B de Geus1, H HogenEsch, R T Kubo
1Section of Immunology, TNO Institute of Aging and Vascular Research, Leiden, The Netherlands.
Murine intestinal intraepithelial lymphocytes (ilEL) represent a heterogeneous population of cells which contains both TCR alpha beta+ and TCR gamma delta+ cells. In contrast to the TCR alpha beta+ cell population in peripheral lymphoid organs, the TCR alpha beta+ ilEL contain high numbers of Thy-1- cells. This negativity of ilEL for Thy-1, a glycosylphosphatidyl inositol (GPI)-linked membrane protein, is not the result of conformational changes of the Thy-1 molecule. The absence of Thy-1 on TCR gamma delta+ and a subset of TCR alpha beta+ ilEL is furthermore not caused by a general defect in the processing of GPI-linked proteins, since Thy-1- ilEL mainly express another GPI-linked protein, Qa-2. However, TCR alpha beta+ and TCR gamma delta+ ilEL are also virtually negative for two other members of this family of activation-associated GPI-linked proteins, Ly-6A and Ly-6C. This unusual pattern of GPI-linked protein expression on TCR+ ilEL may be related to differences in cellular activation and signal transduction pathways between TCR+ ilEL and regular peripheral T cells.
Murine intestinal intraepithelial lymphocytes (ilEL) represent a heterogeneous population of cells which contains both TCR alpha beta+ and TCR gamma delta+ cells. In contrast to the TCR alpha beta+ cell population in peripheral lymphoid organs, the TCR alpha beta+ ilEL contain high numbers of Thy-1- cells. This negativity of ilEL for Thy-1, a glycosylphosphatidyl inositol (GPI)-linked membrane protein, is not the result of conformational changes of the Thy-1 molecule. The absence of Thy-1 on TCR gamma delta+ and a subset of TCR alpha beta+ ilEL is furthermore not caused by a general defect in the processing of GPI-linked proteins, since Thy-1- ilEL mainly express another GPI-linked protein, Qa-2. However, TCR alpha beta+ and TCR gamma delta+ ilEL are also virtually negative for two other members of this family of activation-associated GPI-linked proteins, Ly-6A and Ly-6C. This unusual pattern of GPI-linked protein expression on TCR+ ilEL may be related to differences in cellular activation and signal transduction pathways between TCR+ ilEL and regular peripheral T cells.
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