Class II Major Histocompatibility Complex Antigen Expression and Cellular Interactions in Thyroid Glands of Graves' Disease

Matsunaga, Mayumi; Eguchi, Katsumi; Fukuda, Takaaki; Kurata, Akihiko; Tezuka, Hiroshi; Shimomura, C; Otsubo, Tempei; Ishikawa, Naofumi; Ito, Kunihiko; Nagataki, Shigenobu

doi:10.1210/jcem-62-4-723

Cited by 76 publications

(29 citation statements)

References 20 publications

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“…We also observed that the concentration of FCS did not influence the levels of sICAM-1 which were identical with 10% FCS or 10% NU-serum, a synthetic product containing only 1% serum. These results corroborate those of Ciampolillo et al (1993) who tested only membrane ICAM-1 culture Several reports have been published on human thyrocytes cocultured in monolayers with autologous PBL or ITL lymphocytes (Davies et al 1985, Iwatani et al 1986, Matsunaga et al 1986, Otsubo et al 1988, Sato et al 1993, Massart et al 1995, 1996. However, our present work is the first demonstration of the action of PBL and ITL cocultured with autologous thyrocytes on the expression of membrane and soluble ICAM-1.…”

Section: Discussionsupporting

confidence: 90%

Expression of membrane and soluble intercellular adhesion molecule-1 in Graves' disease

Massart

Sonnet²,

Gibassier³

et al. 1997

Journal of Molecular Endocrinology

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We have investigated the in vitro expression of membrane and soluble intercellular adhesion molecule-1 (ICAM-1) by human thyroid cells from 20 patients with Graves' disease and 5 normal subjects. Membrane ICAM-1 was not detected by flow cytometry analysis in non-cultured thyrocytes from either normal or Graves' disease tissues. It appeared on thyroid cells after a 24-h culture in monolayers and showed a regular dose-dependent increase. The same results were obtained with soluble ICAM-1 (sICAM-1) in culture media from cells cultured in monolayers, vesicles or follicles. No change was obtained with different concentrations of fetal calf serum added to the media. Coculture of Graves' disease thyrocytes with autologous peripheral blood lymphocytes (PBL) or intrathyroidal lymphocytes (ITL) enhanced the expression of both membrane and sICAM-1 whatever the culture model. When normal thyrocytes were cocultured with PBL, sICAM-1 increased but with ITL sICAM-1 remained unchanged. High concentrations of gamma interferon induced an increase of both membrane and sICAM-1 in the three culture models. However the increases were greater with vesicles and follicles. Only sICAM-1 levels were raised with 0·1, 1 and 10 µ retinoic acid. These results suggest that ICAM-1 appears in culture, possibly due to mechanical effects such as adherence to plates and cell-to-cell contacts. Moreover, its expression is modulated by several factors such as cytokines or retinoic acid. Further investigations are needed to establish whether ICAM-1 is really involved in the pathogenesis of Graves' disease.

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Section: Discussionsupporting

confidence: 90%

Expression of membrane and soluble intercellular adhesion molecule-1 in Graves' disease

Massart

Sonnet²,

Gibassier³

et al. 1997

Journal of Molecular Endocrinology

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“…TFC from autoimmune thyroid diseased glands have been shown to be capable of presenting autoantigens lo self-reactive lymphocytes and to enhance the activation of autologous lymphocytes [24][25][26]. Additionally, it has been demonstrated that susceptibility to killing by cytotoxic T cells is dependent on the level of MHC class I expression by the target cell [27].…”

Section: Discussionmentioning

confidence: 99%

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Atta

Irving

Powell

et al. 1995

Clinical and Experimental Immunology

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SUMMARYCertain viruses are known to modulate the cellular expression of MHC molecules. We have investigated whether reovirus types I or 3 can alter the normal MHC molecule expression on cultured human thyroid follicular cells (TFC). Primary TFC cultures were established from eight human thyroid donors and MHC class I and II expression was assessed by indirect immunofluorescence microscopy. Both types ot" reovirus enhanced MHC class 1 expression on TFC from all thyroid donors. Class II MHC prolein was strongly induced by type 1 reovirus on TFC from one donor, while weak induction of expression, by either reo-l or reo-3 virus, was noted on the TFC of five other donors. Studies on the mechanism(s) of MHC class I hyperexpression showed that mouse MoAb against the type 3 reovirus haemagglutinin {anti-HA3) reduced the ability ofthe virus to induce hyperexpression of class I MHC molecules on TFC. However, supernatant harvested from type 3 reovirus-infected TFC cultures maintained its ability to enhance class I expression after incubation with anti-HA3. Moreover, adding rabbit anti-sera lo interferon-alpha (IFN-a) or IFN-/? inhibited the increased class 1 MHC expression on TFC by both types of reovirus. These data suggest that reoviruses (types I and 3) can enhance MHC class I on cultured TFC. The mechanism of MHC class I enhancement is most probably through the release of IFN-cv and lFN-/y.

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“…For IL-1 treatment in the Western blot analyses, each cell line was treated with recombinant human IL-1 (10 ng/ml) for 48 h without FCS for NIM1 cells and with 10% FCS for NPA cells. The methods of preparing thyrocytes from patients with Graves' disease, which we used as a negative control in Western blot analyses, are described in detail elsewhere (Matsunaga et al 1986). …”

Section: Cell Culturementioning

confidence: 99%

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

Zeki¹,

Morimoto²,

Arao³

et al. 1999

Journal of Endocrinology

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This study provides the first report that the same cytokine (interleukin-1 (IL-1)) can induce opposite effects on cyclin-dependent kinases (Cdks) and Cdk inhibitors (Cdkis) in the G 1 phase even in the same type of cancer cells (papillary thyroid carcinoma cells). Cell cycle analysis revealed an increase in NIM1 cells and a decrease in NPA cells in the S and G 2 +M phases after treatment with IL-1 . The addition of IL-1 to NIM1 cells reduced the expression of p16 and p21 protein and induced the expression of Cdk2 and Cdk4 protein, which leads to the phosphorylation of retinoblastoma protein. The addition of IL-1 to NPA cells induced the expression of p27 protein and reduced the expression of Cdk2 protein, which leads to induction of p107 protein expression. It is of interest that p21 protein expression was not observed in NPA cells. These results suggest that several Cdks and Cdkis play a regulatory role in the G 1 cell cycle progression and arrest induced by IL-1 in thyroid carcinoma cell lines.

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Class II Major Histocompatibility Complex Antigen Expression and Cellular Interactions in Thyroid Glands of Graves' Disease

Cited by 76 publications

References 20 publications

Expression of membrane and soluble intercellular adhesion molecule-1 in Graves' disease

Expression of membrane and soluble intercellular adhesion molecule-1 in Graves' disease

Enhanced expression of MHC class I molecules on cultured human thyroid follicular cells infected with reovirus through induction of type 1 interferons

Interleukin-1alpha regulates G1 cell cycle progression and arrest in thyroid carcinoma cell lines NIM1 and NPA

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