Helicobacter Pylori-Specific Tumour-Infiltrating T Cells Provide Contact Dependent Help for the Growth of Malignant B Cells in Low-Grade Gastric Lymphoma of Mucosa-Associated Lymphoid Tissue

Hussell, Tracy; Isaacson, Peter G.; Crabtree, Jean E.; Spencer, Jo

doi:10.1002/(sici)1096-9896(199602)178:2<122::aid-path486>3.0.co;2-d

Cited by 332 publications

(182 citation statements)

References 22 publications

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“…3 The tumor cells of low-grade gastric MALT lymphoma are memory B lymphocytes still responsive to differentiation signals, such as CD40 costimulation and cytokines produced by antigenstimulated T-helper (Th) cells, 4 and their growth depends on stimulation by H. pylori-specific T cells. 5,6 In early phases, this tumor is sensitive to withdrawal of H. pylori-induced T-cell help, providing an explanation for both the tumor's tendency to remain localized to the primary site and its regression after H. pylori is eradicated with antibiotics. 7,8 Tumor growth may depend on evasion from T cellmediated cytotoxicity.…”

mentioning

confidence: 99%

Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma

D’Elios¹,

Amedei²,

Manghetti³

et al. 1999

Gastroenterology

100

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mentioning

confidence: 99%

Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma

D’Elios¹,

Amedei²,

Manghetti³

et al. 1999

Gastroenterology

100

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“…Therefore, the malfunction of apoptosis could explain the insensitivity of malignant B cells toward T cell control that may exist in vitro and in vivo Hussell et al, 1996;Knörr et al, 1999). In our study, we measured T cell-induced, Fas-mediated apoptosis in malignant B cells in vitro and compared it with normal memory B cells under the same experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…In recent studies, the gene for the human inhibitor of apoptosis protein-1 (HIAP-1) on chromosome 11 was identified as being directly affected by this translocation (Dierlamm et al, 1999). The protein HIAP-1 has been implicated in Fas-induced apoptosis and other death pathways by direct inhibition of some caspases (Deveraux and Reed, 1999;Deveraux et al, 1998;Roy et al, 1997).Therefore, the malfunction of apoptosis could explain the insensitivity of malignant B cells toward T cell control that may exist in vitro and in vivo Hussell et al, 1996;Knörr et al, 1999). In our study, we measured T cell-induced, Fas-mediated apoptosis in malignant B cells in vitro and compared it with normal memory B cells under the same experimental conditions.…”

mentioning

confidence: 99%

Loss of Fas (CD95/APO-1) Regulatory Function Is an Important Step in Early MALT-Type Lymphoma Development

Seeberger

Starostik

Schwarz

et al. 2001

Laboratory Investigation

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SUMMARY:Fas (CD95, APO-1) mutations were found in autoimmune diseases and some lymphomas, suggesting impairment of Fas-mediated cell death signaling that may cause tumor development. Because mucosa-associated lymphoid tissue (MALT)-type lymphoma B cells recognize autoantigens and proliferate in response to antigen and T cell-mediated signals, it is suggestive that autoreactive B cell lymphoma precursor cells may have escaped the Fas-mediated checkpoint that normally operates in healthy individuals. Using different biochemical, molecular, and functional approaches, we analyzed the Fas signaling in malignant B cells from seven MALT-type lymphomas that were additionally characterized for the t(11;18)(q21;q21) and four gastric diffuse large B cell lymphomas (DLBL). All DLBLs and three of seven MALT-type lymphomas were resistant to Fas-mediated apoptosis in vitro. Moreover, four of five MALT-type lymphomas analyzed and one of three DLBLs analyzed showed mutations in Fas mRNA transcripts but no loss of heterozygosity in the Fas promotor region. Alternative mechanisms of resistance to apoptosis, such as decreased expression of Fas or production of soluble Fas were not operative. Therefore, it is suggestive that a subgroup of MALT-type lymphoma B cells, irrespective of t(11;18)(q21;q21), escape the censoring Fas pathway by mutating and inactivating Fas. This identifies a key regulatory step in early MALT-type lymphomagenesis. (Lab Invest 2001, 81:977-986).M arginal zone B cell lymphomas of mucosaassociated lymphoid tissue (MALT)-type are neoplastic counterparts of normal memory B cells (Harris et al, 1994). The development from naive to memory B cells is closely accompanied and regulated by T cells through Fas/FasL interaction (Nagata, 1997;Suda et al, 1993) taking place in the germinal centers of follicles and leading either to deletion of autoantigen-recognizing B cells or to further differentiation into memory B cells resident in the marginal zone of the follicle (Goodnow, 1996;Rathmell et al, 1996) and plasma cells. Therefore, disruption of the Fas/FasL apoptotic pathway is associated with lymphoproliferative and autoimmune disorders as demonstrated in mice carrying lymphoproliferation (lpr) or generalized lymphoproliferative disease (gld) mutations affecting the genes for Fas and FasL, respectively (Takahashi et al, 1994;Watanabe-Fukunaga et al, 1992), or in humans carrying inherited mutations in the Fas gene leading to autoimmune lymphoproliferative syndrome (Bettinardi et al, 1997;Fisher et al, 1995;Rieux Laucat et al, 1995;Sneller et al, 1997). Because autoantigen receptors and marginal zone B cell expansions are characteristic features of MALT-type lymphoma , we searched for a link between tumor development and functionality of the Fas/FasL apoptotic pathway. In addition, the translocation t(11;18)(q21;q21) is the most characteristic chromosomal aberration in extranodal MALT-type lymphoma and may interfere with the regulation of apoptosis. In recent studies, the gene for the human inhibitor of apoptosis protein...

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“…The microenvironment of the inflammatory cells in LIP may activate B cells and contribute to the development of a monoclonal B-cell population. Analogous to Helicobacter pylori lymphocytic chronic gastritis and gastric MALT lymphoma, or myoepithelial sialadenitis and salivary gland MALT lymphoma (24,25), LIP may therefore represent an early stage or a precursor lesion of pulmonary MALT lymphoma.…”

Section: Discussionmentioning

confidence: 99%

Chemokine Gene Expression and Clonal Analysis of B Cells in Tissues Involved by Lymphoid Interstitial Pneumonitis from HIV-Infected Pediatric Patients

et al. 2001

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Helicobacter Pylori-Specific Tumour-Infiltrating T Cells Provide Contact Dependent Help for the Growth of Malignant B Cells in Low-Grade Gastric Lymphoma of Mucosa-Associated Lymphoid Tissue

Cited by 332 publications

References 22 publications

Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma

Impaired T-cell regulation of B-cell growth in Helicobacter pylori–related gastric low-grade MALT lymphoma

Loss of Fas (CD95/APO-1) Regulatory Function Is an Important Step in Early MALT-Type Lymphoma Development

Chemokine Gene Expression and Clonal Analysis of B Cells in Tissues Involved by Lymphoid Interstitial Pneumonitis from HIV-Infected Pediatric Patients

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