Induction of intercellular adhesion molecule-1 but not of lymphocyte function-associated antigen-3 in thyroid follicular cells
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Induction of intercellular adhesion molecule-1 but not of lymphocyte function-associated antigen-3 in thyroid follicular cells. / Tolosa, E; Roura, C; Martí, M; Belfiore, A; Pujol-Borrell, R.
In: J AUTOIMMUN, Vol. 5, No. 1, 01.02.1992, p. 119-35.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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T1 - Induction of intercellular adhesion molecule-1 but not of lymphocyte function-associated antigen-3 in thyroid follicular cells
AU - Tolosa, E
AU - Roura, C
AU - Martí, M
AU - Belfiore, A
AU - Pujol-Borrell, R
PY - 1992/2/1
Y1 - 1992/2/1
N2 - We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3) by thyrocytes and their regulation by cytokines. Immunofluorescence studies on cryostat sections and on freshly dispersed cell preparations showed that ICAM-1 and LFA-3 are barely detectable in non-autoimmune thyrocytes. However, thyrocytes acquired ICAM-1 expression in culture. IFN-gamma, IL-1 beta and TNF-alpha produced a clear enhancement of ICAM-1 expression. When tested in combination, IL-1 beta and TNF-alpha were additive to the IFN-gamma effect. LFA-3 expression was not modulated by these cytokines. In the HT93 thyroid cell line generated by transfection with SV40, ICAM-1 and LFA-3 were both constitutively expressed at high levels. Cytokines modulated ICAM-1 expression similarly, but to a greater extent than in normal thyrocytes. LFA-3 remained unmodified. These results support the notion that normal thyrocytes are immunologically silent cells. The capability of cytokines to induce ICAM-1 together with HLA class I and class II-expression on thyrocytes suggests that under their influence, these cells may express all the surface molecules required for antigen presentation and/or for being recognized as target cells in the context of thyroid autoimmune disease.
AB - We investigated the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-3 (LFA-3) by thyrocytes and their regulation by cytokines. Immunofluorescence studies on cryostat sections and on freshly dispersed cell preparations showed that ICAM-1 and LFA-3 are barely detectable in non-autoimmune thyrocytes. However, thyrocytes acquired ICAM-1 expression in culture. IFN-gamma, IL-1 beta and TNF-alpha produced a clear enhancement of ICAM-1 expression. When tested in combination, IL-1 beta and TNF-alpha were additive to the IFN-gamma effect. LFA-3 expression was not modulated by these cytokines. In the HT93 thyroid cell line generated by transfection with SV40, ICAM-1 and LFA-3 were both constitutively expressed at high levels. Cytokines modulated ICAM-1 expression similarly, but to a greater extent than in normal thyrocytes. LFA-3 remained unmodified. These results support the notion that normal thyrocytes are immunologically silent cells. The capability of cytokines to induce ICAM-1 together with HLA class I and class II-expression on thyrocytes suggests that under their influence, these cells may express all the surface molecules required for antigen presentation and/or for being recognized as target cells in the context of thyroid autoimmune disease.
KW - Antibodies, Monoclonal
KW - Antigens, CD58
KW - Antigens, Surface
KW - Blotting, Northern
KW - Cell Adhesion Molecules
KW - Cell Line
KW - Cytokines
KW - Female
KW - Flow Cytometry
KW - Fluorescent Antibody Technique
KW - Goiter, Nodular
KW - HLA-DR Antigens
KW - Histocompatibility Antigens Class I
KW - Humans
KW - Intercellular Adhesion Molecule-1
KW - Membrane Glycoproteins
KW - Thyroid Gland
M3 - SCORING: Journal article
C2 - 1373059
VL - 5
SP - 119
EP - 135
JO - J AUTOIMMUN
JF - J AUTOIMMUN
SN - 0896-8411
IS - 1
ER -