Significance of the expression of major histocompatibility complex class II antigen, HLA‐DR and ‐DQ, with recurrence of papillary thyroid cancer

Jo, Young Suk; Lee, Jun Chul; Li, Shengjin; Choi, Yun-Sun; Bai, Youn-Sun; Kim, Yun-Jeung; Lee, Ihn-Suk; Rha, So Young; Ro, Heung-Kyu; Kim, Jin Man; Shong, Minho

doi:10.1002/ijc.23167

Cited by 26 publications

(25 citation statements)

References 28 publications

(36 reference statements)

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“…On the contrary, several female cells either CD45 + or Tg + expressed MHC II antigen, consistent with a role as antigenpresenting cells. Indeed, tumoral follicular cells, but not normal thyroid cells, have been shown to harbor the aberrant expression of MHC II antigen, which is believed to be triggered by oncogenes, such as ret/PTC, and to have an immunomodulatory function (25). Thus, the lack of MHC II expression in Tg + male cells argues against a transformed phenotype and a role as antigen-presenting cells, supporting instead a possible function in the replacement of damaged cells and repair of the thyroid tissue.…”

Section: Discussionmentioning

confidence: 99%

Fetal Cell Microchimerism in Papillary Thyroid Cancer: A Possible Role in Tumor Damage and Tissue Repair

et al. 2008

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Fetal cells enter the maternal circulation during pregnancy and can persist in the maternal blood or tissues for decades, creating a physiologic microchimerism. Because papillary thyroid cancer (PTC) is more frequent in women, the role of persisting fetal male cells in this tumor has been investigated. Tumor tissue specimens were obtained from 63 women with PTC who had a male pregnancy before the diagnosis. Male cells, identified by PCR amplification of a male-specific gene, the sex-determining region Y, was detected in 47.5% of women. By fluorescence in situ hybridization (FISH) analyses, the total number of microchimeric cells was significantly higher in neoplastic tissue than in controlateral normal sections. By combined FISH and immunohistochemistry (immuno-FISH), male cells expressing thyroglobulin were found in tumor and normal tissues, whereas male microchimeric cells stained with the CD45 antigen were detected only in tumor sections. Microchimeric cells negative for either marker were detected both in tumor and normal tissues. Moreover, both CD45 + and Tg + fetal cells did not express MHC II antigens. In conclusion, fetal microchimerism has been documented in a high proportion of women with PTC. The immuno-FISH studies indicate that CD45

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Section: Discussionmentioning

confidence: 99%

Fetal Cell Microchimerism in Papillary Thyroid Cancer: A Possible Role in Tumor Damage and Tissue Repair

et al. 2008

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“…12 The frequency of these changes varies among the different types of hematopoietic and solid tumors depending on their origin and/or molecular phenotype 23,30,31 : for example, more than 80% of ductal breast carcinoma lesions analyzed lack HLA class II antigen expression. 29,30 In contrast, about 50% of papillary thyroid carcinoma and 60% of primary melanoma express HLA class II antigens 31,32 suggesting a gain of HLA class II antigen expression in these tumor types. In addition, a heterogeneous intra-tumoral HLA class II antigen expression pattern was detected in HLA class II antigen-positive tumor lesions.…”

Section: Expression Of Hla Class II Antigens In Malignant Tumorsmentioning

confidence: 99%

HLA class II antigen-processing pathway in tumors: Molecular defects and clinical relevance

2017

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The human leukocyte antigen (HLA) class II antigen-processing machinery (APM) presents to cognate CD4 C T-cells antigenic peptides mainly generated from exogeneous proteins in the endocytic compartment. These CD4 C T cells exert helper function, but may also act as effector cells, thereby recognizing HLA class II antigen-expressing tumor cells. Thus, HLA class II antigen expression by tumor cells influences the tumor antigen (TA)-specific immune responses and, depending on the cancer type, the clinical course of the disease. Many types of human cancers express HLA class II antigens, although with marked differences in their frequency. Some types of cancer lack HLA class II antigen expression, which could be due to structural defects or deregulation affecting different components of the complex HLA class II APM and/or from lack of cytokine(s) in the tumor microenvironment. In this review, we have summarized the information about HLA class II antigen distribution in normal tissues, the structural organization of the HLA class II APM, their expression and regulation in malignant cells, the defects, which have been identified in malignant cells, and their functional and clinical relevance.

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“…MHC class II molecules are expressed by professional antigen presenting cells (APCs), such as dendritic cells (DCs) and B cells, as well as cancers derived from these cell types. In addition, ectopic expression of MHC class II has been described on multiple cancers, including melanoma, breast, colon, thyroid, and cervical (6, 13–16). Therefore, MHC class II-restricted processing and presentation by tumor cells may exert a major influence over T cell responses and play a critical role in anti-tumor immunity.…”

Section: Introductionmentioning

confidence: 99%

Low GILT Expression is Associated with Poor Patient Survival in Diffuse Large B-Cell Lymphoma

et al. 2013

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The major histocompatibility complex (MHC) class II-restricted antigen processing pathway presents antigenic peptides acquired in the endocytic route for the activation of CD4+ T cells. Multiple cancers express MHC class II, which may influence the anti-tumor immune response and patient outcome. Low MHC class II expression is associated with poor survival in diffuse large B-cell lymphoma (DLBCL), the most common form of aggressive non-Hodgkin lymphoma. Therefore, we investigated whether gamma-interferon-inducible lysosomal thiol reductase (GILT), an upstream component of the MHC class II-restricted antigen processing pathway that is not regulated by the transcription factor class II transactivator, may be important in DLBCL biology. GILT reduces protein disulfide bonds in the endocytic compartment, exposing additional epitopes for binding to MHC class II and facilitating antigen presentation. In each of four independent gene expression profiling cohorts with a total of 585 DLBCL patients, low GILT expression was significantly associated with poor overall survival. In contrast, low expression of a classical MHC class II gene, HLA-DRA, was associated with poor survival in one of four cohorts. The association of low GILT expression with poor survival was independent of established clinical and molecular prognostic factors, the International Prognostic Index and the cell of origin classification, respectively. Immunohistochemical analysis of GILT expression in 96 DLBCL cases demonstrated variation in GILT protein expression within tumor cells which correlated strongly with GILT mRNA expression. These studies identify a novel association between GILT expression and clinical outcome in lymphoma. Our findings underscore the role of antigen processing in DLBCL and suggest that molecules targeting this pathway warrant investigation as potential therapeutics.

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Significance of the expression of major histocompatibility complex class II antigen, HLA‐DR and ‐DQ, with recurrence of papillary thyroid cancer

Cited by 26 publications

References 28 publications

Fetal Cell Microchimerism in Papillary Thyroid Cancer: A Possible Role in Tumor Damage and Tissue Repair

Fetal Cell Microchimerism in Papillary Thyroid Cancer: A Possible Role in Tumor Damage and Tissue Repair

HLA class II antigen-processing pathway in tumors: Molecular defects and clinical relevance

Low GILT Expression is Associated with Poor Patient Survival in Diffuse Large B-Cell Lymphoma

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