Role of activated host T cells in the promotion of MALT lymphoma growth

Guindi, Maha

doi:10.1006/scbi.2000.0351

Cited by 13 publications

(6 citation statements)

References 27 publications

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“…Although, the role of TLRs in the pathogenesis of MALT lymphoma has been poorly investigated, the immune response to chronic stimulation by H. pylori infection is thought to induce NFκB activation in B cells, which plays a crucial part in the development of MALT lymphoma (83, 84). In addition, the presentation of H. pylori by dendritic cells recruits and activates T cell responses, which enhance B cell activation through CD40–CD40L interactions (85) (Figure 3A). Thus, both direct activation of TLR signaling by H. pylori and T cell-mediated B cell activation could be involved in the pathogenesis of MALT lymphoma (86).…”

Section: Helicobacter Pylori Inflammation and Malt Lymphomamentioning

confidence: 99%

Toll-Like Receptors and Cancer: MYD88 Mutation and Inflammation

et al. 2014

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Pattern recognition receptors (PRRs) expressed on immune cells are crucial for the early detection of invading pathogens, in initiating early innate immune response and in orchestrating the adaptive immune response. PRRs are activated by specific pathogen-associated molecular patterns that are present in pathogenic microbes or nucleic acids of viruses or bacteria. However, inappropriate activation of these PRRs, such as the Toll-like receptors (TLRs), due to genetic lesions or chronic inflammation has been demonstrated to be a major cause of many hematological malignancies. Gain-of-function mutations in the TLR adaptor protein MYD88 found in 39% of the activated B cell type of diffuse large B cell lymphomas and almost 100% of Waldenström’s macroglobulinemia further highlight the involvement of TLRs in these malignancies. MYD88 mutations result in the chronic activation of TLR signaling pathways, thus the constitutive activation of the transcription factor NFκB to promote cell survival and proliferation. These recent insights into TLR pathway driven malignancies warrant the need for a better understanding of TLRs in cancers and the development of novel anti-cancer therapies targeting TLRs. This review focuses on TLR function and signaling in normal or inflammatory conditions, and how mutations can hijack the TLR signaling pathways to give rise to cancer. Finally, we discuss how potential therapeutic agents could be used to restore normal responses to TLRs and have long lasting anti-tumor effects.

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Section: Helicobacter Pylori Inflammation and Malt Lymphomamentioning

confidence: 99%

Toll-Like Receptors and Cancer: MYD88 Mutation and Inflammation

et al. 2014

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“…Meanwhile, CD86 positive MALT lymphomas also showed significantly increased infiltration of CD56 (+) NK cells compared to CD86-negative cases (2.9±1.1% vs 1.4±1.3%; P = 0.005). T-cells [23] . However, the precise role of CD80 and CD86 molecules in the signaling of B-cells remains unclear.…”

Section: Correlation Of Expression Of Cd86 and Infiltration Of Cd56 (mentioning

confidence: 99%

Expression of CD86 and increased infiltration of NK cells are associated withHelicobacter pylori-dependent state of early stage high-grade gastric MALT lymphoma

Kuo

Chen

Chen³

et al. 2005

WJG

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Abstract Abstract AbstractAIM: A high percentage of early-stage high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori (H pylori)-dependent. However, unlike their low-grade counterparts, high-grade gastric MALT lymphomas may progress rapidly if unresponsive to H pylori eradication. It is mandatory to identify markers that may predict the H pylori-dependent status of these tumors. Proliferation of MALT lymphoma cells depends on cognate help and cell-to-cell contact of H pylori-specific intratumoral T-cells. To examine whether the expression of co-stimulatory marker CD86 (B7.2) and the infiltration of CD56 (+) natural killer (NK) cells can be useful markers to predict H pylori-dependent status of high-grade gastric MALT lymphoma. METHODS:Lymphoma biopsies from 26 patients who had participated in a prospective study of H pylori-eradication for stage I E high-grade gastric MALT lymphomas were evaluated. Tumors that resolved to Wotherspoon grade II or less after H pylori eradication were classified as H pyloridependent; others were classified as H pylori-independent. The infiltration of NK cells and the expression of CD86 in pre-treatment paraffin-embedded lymphoma tissues were determined by immunohistochemistry. RESULTS:There were 16 H pylori-dependent and 10 H pylori-independent cases. CD86 expression was detected in 11 (68.8%) of 16 H pylori-dependent cases but in none of 10 H pylori-independent cases (P = 0.001). H pylori-dependent high-grade gastric MALT lymphomas contained significantly higher numbers of CD56 (+) NK cells than H pylori-independent cases (2.8±1.4% vs 1.1±0.8%; P = 0.003). CD86 positive MALT lymphomas also showed significantly increased infiltration of CD56 (+) NK cells compared to CD86-negative cases (2.9±1.1% vs 1.4±1.3%; P = 0.005). CONCLUSION:These results suggest that the expression of co-stimulatory marker CD86 and the increased infiltration of NK cells are associated with H pylori-dependent state of early-stage high-grade gastric MALT lymphomas.

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“…All these data suggest that OM can have effects other than the known therapeutic ones and can affect cells other than those of the gastric mucosa. Since it has also been demonstrated that OM has an antinflammatory activity on cellular infiltrate arising when there is gastric ulcer and Helicobacter pylori associated gastritis (27)(28)(29)(30)(31)(32) we considered it important to analyze the effect of the drug on T lymphocytes using aT cell line as a model.…”

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confidence: 99%

Omeprazole Induces Apoptosis in Jurkat Cells

Scaringi

Cornacchione

Ayroldi

et al. 2004

Int J Immunopathol Pharmacol

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We report for the first time a potent apoptotic effect of omeprazole (OM). Apoptosis was induced in Jurkat cells in a time and concentration-dependent mode. Caspase 3 and PARP were rapidly cleaved in response to OM, but apoptosis was only partially inhibited by the caspase 3 inhibitor DEVD-CHO. OM also induced an early lysosomal destabilization which increased progressively and was correlated with a parallel increase in apoptotic cells. The cysteine protease inhibitor E64d gave strong protection against apoptosis thus proving the involvement oflysosomal enzymes in OM-induced apoptosis whereas, it did not impede the caspase 3 cleavage. Instead ZVAD-fmk, a general caspase inhibitor, also able to inhibit cathepsin activity, protected cells completely from OM-induced apoptosis. It therefore seems that both caspases and cysteine cathepsins are involved in the execution stage of OM-induced apoptosis.

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Role of activated host T cells in the promotion of MALT lymphoma growth

Cited by 13 publications

References 27 publications

Toll-Like Receptors and Cancer: MYD88 Mutation and Inflammation

Toll-Like Receptors and Cancer: MYD88 Mutation and Inflammation

Expression of CD86 and increased infiltration of NK cells are associated withHelicobacter pylori-dependent state of early stage high-grade gastric MALT lymphoma

Omeprazole Induces Apoptosis in Jurkat Cells

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