Tumour infiltrating T-cells in gastric lymphoma

Hussell, Tracy; Isaacson, Peter G.; Spencer, Jo

doi:10.1007/bf00194691

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…T lymphocytes were diffusely infiltrating the mucosal layer and intermingling among the lymphoma cells, as reported previously 21–23,25 , 28–32 . We support that infiltrating T cells may play a role in pathogenesis of MALT lymphoma.…”

Section: Discussionsupporting

confidence: 90%

“…The response of low‐grade B‐cell gastric MALT lymphomas to stimulating strains of H. pylori is dependent on H. pylori ‐specific T cells and their products rather than the bacteria themselves 1,21–24 . Yoshino and Akagi reported that autoreactive B cells proliferate in response to H. pylori ‐specific T cells, presumably with some cytokines 25 .…”

Section: Discussionmentioning

confidence: 99%

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MUC1 mucin expression in follicular dendritic cells and lymphoepithelial lesions of gastric mucosa‐associated lymphoid tissue lymphoma

Taki

Kitajima

Sueyoshi

et al. 2002

Pathology International

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Membrane-associated mucin MUC1 is expressed in various adenocarcinoma cells and active T lymphocytes. We tried to find out whether MUC1 is expressed in gastric mucosa-associated lymphoid tissue (MALT) lymphoma lesion. MUC1 was not expressed in infiltrating T lymphocytes; however, MUC1 was found on the cell surface of follicular dendritic cells (FDC) of germinal centers and in the epithelial cytoplasm of lymphoepithelial lesion (LEL) of the lymphoma, which were immunohistochemically detected by monoclonal antibodies DF3 and MY.1E12. MUC1 was also expressed in the FDC of control cases (gastrectomy specimen containing reactive lymphoid follicles, n = 10, MUC1/ DF3, 100%; MUC1/MY.1E12, 40%), and FDC in MALT lymphomas (n = 59) showed lower MUC1 expression rates (MUC1/ DF3, 32%; MUC1/MY.1E12, 0%) than the control (P < 0.001). Lymphoepithelial lesion in the low-grade MALT lymphomas (n = 23) showed a higher MUC1/DF3 expression rate (30%) than those in the high-grade MALT lymphomas (n = 36; 6%; P < 0.05). T lymphocytes in the surface mucosa were more frequent in MALT lymphoma (91.4 +/- 80.6/unit area) than those in the control (20.0 +/- 23.6) (P < 0.001). S100-positive dendritic cells around LEL were more frequent in the low-grade (19.0 +/- 9.4/unit area) than in the high-grade (11.7 +/- 9.7) (P < 0.005). This study demonstrated MUC1 mucin expression on FDC for the first time. Mucosa-associated lymphoid tissue lymphoma, especially low-grade, shows immunologically active state, where FDC MUC1 expression may be suppressed by some factors released from lymphoma cells. Further study to elucidate the pathogenetic role of MUC1 in MALT lymphoma is necessary.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

MUC1 mucin expression in follicular dendritic cells and lymphoepithelial lesions of gastric mucosa‐associated lymphoid tissue lymphoma

Taki

Kitajima

Sueyoshi

et al. 2002

Pathology International

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“…2,3 Low-grade MALT lymphoma is initially confined to the gastric mucosa, and its growth depends critically on the contact help of H pylori-specific intratumoral T cells; therefore, it responds favorably to H pylori eradication therapy. [4][5][6] However, when the lymphoma invades the deep layers of the gastric wall and disseminates to local lymph nodes and distal sites, the tumor loses its dependence on H pylori-specific T cells and is no longer sensitive to H pylori eradication therapy. [7][8][9] Finally, low-grade gastric MALT lymphoma may transform into a more aggressive diffuse large B-cell lymphoma (DLBCL).…”

Section: Introductionmentioning

confidence: 99%

“…[7][8][9] Finally, low-grade gastric MALT lymphoma may transform into a more aggressive diffuse large B-cell lymphoma (DLBCL). 10,11 Direct 12-14 and indirect antigen stimulation 4,5 and several genetic factors, including genetic instability, 15 trisomy 3, 16 p53 mutation/LOH, 17 p16 deletion, 18 t(1;14)(p22;q32), 19 and t(11; 18)(q21;q21), 20,21 are implicated in MALT lymphoma development. However, the molecular events underlying the multistep progression of the tumor remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

T(11;18)(q21;q21) is associated with advanced mucosa-associated lymphoid tissue lymphoma that expresses nuclear BCL10

Liu

Doğan

et al. 2001

Blood

229

197

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The development of gastric mucosaassociated lymphoid tissue (MALT) lymphoma is a multistep process and can be clinico-pathologically divided into Helicobacter pylori-associated gastritis, lowgrade tumors, and high-grade tumors. The molecular events underlying this progression are largely unknown. However, identification of the genes involved in MALT lymphoma-specific t(11;18)(q21; q21) and t(1;14)(p22;q32) has provided fresh insights into the pathogenesis of this disease. T(11;18)(q21;q21) results in a chimeric transcript between the API2 and the MALT1 genes, whereas t(1;14) (p22;q32) causes aberrant nuclear BCL10 expression. Significantly, nuclear BCL10 expression also occurs frequently in MALT lymphomas without t(1;14)(p22; q32), suggesting an important role for BCL10 in lymphoma development. Thirtythree cases of H pylori gastritis, 72 MALT lymphomas, and 11 mucosal diffuse large B-cell lymphomas (DLBCL) were screened for t(11;18)(q21;q21) by reverse transcription-polymerase chain reaction followed by sequencing. BCL10 expression in lymphoma cases was examined by immunohistochemistry. The API2-MALT1 fusion transcript was not detected in H pylori gastritis and mucosal DLBCL but was found in 25 of 72 (35%) MALT lymphomas of various sites. Nuclear BCL10 expression was seen in 28 of 53 (53%) of MALT lymphomas. Of the gastric cases, the largest group studied, the frequency of both t(11;18)(q21;q21) and nuclear BCL10 expression was significantly higher in tumors that showed dissemination to local lymph nodes or distal sites (14 of 18 ‫؍‬ 78% and 14 of 15 ‫؍‬ 93%, respectively) than those confined to the stomach (3 of 29 ‫؍‬ 10% and 10 of 26 ‫؍‬ 38%). Furthermore, t(11;18)(q21;q21) closely correlated with BCL10 nuclear expression. These results indicate that both t(11;18)(q21;q21) and BCL10 nuclear expression are associated with advanced MALT lymphoma and that their oncogenic activities may be related to each other. IntroductionThe development of mucosa-associated lymphoid tissue (MALT) lymphoma is a multistage process. 1 This is best understood in gastric MALT lymphoma, the most common form. Typically, low-grade gastric MALT lymphoma arises from mucosal lymphoid tissue that is acquired usually as a reaction to Helicobacter pylori infection. 2,3 Low-grade MALT lymphoma is initially confined to the gastric mucosa, and its growth depends critically on the contact help of H pylori-specific intratumoral T cells; therefore, it responds favorably to H pylori eradication therapy. [4][5][6] However, when the lymphoma invades the deep layers of the gastric wall and disseminates to local lymph nodes and distal sites, the tumor loses its dependence on H pylori-specific T cells and is no longer sensitive to H pylori eradication therapy. 7-9 Finally, low-grade gastric MALT lymphoma may transform into a more aggressive diffuse large B-cell lymphoma (DLBCL). 10,11 Direct 12-14 and indirect antigen stimulation 4,5 and several genetic factors, including genetic instability, 15 trisomy 3, 16 p53 mutation/LOH, 17 p16 deletion, 18 t(1;...

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Oligoclonal Expansions of T-Cell Repertoire in Gastric Mucosa Associated Lymphoid Tissue Type B-Cell Lymphoma and Adjacent Gastritis

Haedicke

Greiner²,

Seeberger³

et al. 1999

Diagnostic Molecular Pathology

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Local stimulation by Helicobacter pylori (HP), autoantigen, and a concurrent T-cell-mediated stimulation of B cells are believed to play an important role in gastric mucosa-associated lymphoid tissue (MALT) type B cell lymphomagenesis. Many autoimmune diseases have shown to lead to a skewed T-cell repertoire with autoantigen specific expansions and deletions. Characterization of lymphoma and gastritis areas of seven gastrectomy specimens using a T-cell receptor beta variable chain (TCR betaV) family-specific reverse transcriptase (RT)-polymerase chain reaction (PCR) assay and fluorescence-activated cell sorter (FACS) analysis revealed a local chronic and acute activation of T cells in lymphoma and an oligoclonal T-cell repertoire in gastritis and in lymphoma, partially sharing the same clones. Local activation and a partial identity suggest that an antigenic challenge caused by a common local pathogen may still continue to take place in MALT type lymphoma as in gastritis, consistent with the view that gastritis may be a precursor lesion of MALT type lymphoma. Expansions that were found only in one of the compartments suggest that also an immune hyperstimulation may contribute to the T-cell repertoire, possibly because of certain tissue antigens. Deletions of TCR betaV families found only in gastritis underline the view that autoantigen may play an important role in its pathogenesis.

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Tumour infiltrating T-cells in gastric lymphoma

Cited by 4 publications

References 19 publications

MUC1 mucin expression in follicular dendritic cells and lymphoepithelial lesions of gastric mucosa‐associated lymphoid tissue lymphoma

MUC1 mucin expression in follicular dendritic cells and lymphoepithelial lesions of gastric mucosa‐associated lymphoid tissue lymphoma

T(11;18)(q21;q21) is associated with advanced mucosa-associated lymphoid tissue lymphoma that expresses nuclear BCL10

Oligoclonal Expansions of T-Cell Repertoire in Gastric Mucosa Associated Lymphoid Tissue Type B-Cell Lymphoma and Adjacent Gastritis

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