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

Taki, Chiaki; Kitajima, Shinichi; Sueyoshi, Kazunobu; Yonezawa, Suguru; Tanaka, Sadao; Sakoda, Koro; Irimura, Tatsuro; Satô, Eiichi; Goto, Masamichi

doi:10.1046/j.1440-1827.2002.01411.x

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…The expression and function of MUC1 in respiratory mucosal epithelial cells are well documented (12). MUC1 expression was also found in immune cells such as T lymphocytes and dendritic cells (20, 21). However, whether MUC1 is functionally expressed in macrophages has not been determined.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, while TNF-α plays a role in MUC1 induction in airway epithelial cells during acute bacterial infection (19), whether it is involved in CS-induced and MUC1-mediated lung cancer development is unknown. Furthermore, it is known that MUC1 is expressed in some immune cells (20, 21), but it is unclear if MUC1 is expressed and functions in macrophages.…”

Section: Introductionmentioning

confidence: 99%

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MUC1 in Macrophage: Contributions to Cigarette Smoke–Induced Lung Cancer

Padilla

et al. 2014

Cancer Research

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Expression of the pro-oncogenic mucin MUC1 is elevated by inflammation in airway epithelial cells, but the contributions of MUC1 to the development of lung cancer are uncertain. In this study, we developed our finding that cigarette smoke (CS) increases Muc1 expression in lung macrophages, where we hypothesized it might contribute to CS-induced transformation of bronchial epithelial cells. In human macrophages, CS extract (CSE) strongly induced MUC1 expression through a mechanism involving the nuclear receptor PPAR-γ. CSE-induced ERK activation was also required for MUC1 expression, but it had little effect on MUC1 transcription. RNAi-mediated attenuation of MUC1 suppressed CSE-induced secretion of TNF-α from macrophages, by suppressing the activity of the TNF-α processing enzyme TACE, arguing that MUC1 is required for CSE-induced and TACE-mediated TNF-α secretion. Similarly, MUC1 blockade after CSE induction through suppression of PPAR-γ or ERK inhibited TACE activity and TNF-α secretion. Conditioned media from CSE-treated macrophages induced MUC1 expression and potentiated CSE-induced transformation of human bronchial epithelial cells (HBEC) in a TNF-α-dependent manner. Together, our results identify a signaling pathway involving PPAR-γ, ERK and MUC1 that is used by CSE to trigger TNF-α secretion from macrophages. Further, our results show how that MUC1 contributes to smoking-induced lung cancers that are driven by inflammatory signals driven by macrophages

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MUC1 in Macrophage: Contributions to Cigarette Smoke–Induced Lung Cancer

Padilla

et al. 2014

Cancer Research

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“…Initial studies focused on the role of T-and NK-cells [2,3], but the growing knowledge about the outstanding role of dendritic cells (DC) in the induction and control of immunity [4] has recently shifted the focus. A clear correlation between clinical outcome and tumor infiltration by DC has been demonstrated for solid and hematologic cancers, including colorectal [5], ovarian [6], gastric [7] and non-small cell lung cancer [8], breast carcinoma [9], oral squamous cell carcinoma [10] and mucosa-associated lymphoid tissue gastric lymphoma [11]. Multiple abnormalities have been reported in peripheral blood (PB) dendritic cells from patients with hematologic diseases including a lower number of circulating myeloid and plasmacytoid DC pre-cursors in multiple myeloma patients [12], the reduction of blood DC counts in CML [13] and the cytogenetic abnormalities in AML DC [14].…”

Section: Introductionmentioning

confidence: 99%

Dendritic cells are significantly reduced in non-Hodgkin's lymphoma and express less CCR7 and CD62L

Fiore

Bergwelt‐Baildon

Drebber

et al. 2006

Leukemia & Lymphoma

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Despite the lack of tumor control, infiltration of immune cells has been demonstrated for several malignancies including non-Hodgkin's lymphoma. Since dendritic cells play a pivotal role in the initiation and control of the immune response, the frequency and phenotype of recently described sub-types of dendritic cells in non-Hodgkin's lymphoma were characterized. Myeloid and plasmacytoid dendritic cells were analysed in 55 non-Hodgkin's lymphoma and 33 reactive lymph nodes by flow cytometry and immunohistochemistry. Overall frequency of dendritic cells in reactive lymph nodes was higher than in non-Hodgkin's lymphoma while the pDC/mDCs ratio was comparable. The low frequency of dendritic cells in infiltrated lymph nodes was confirmed by immunohistochemistry; however, no significant difference in the distribution within lymphoid and tumor tissue was detected. For further characterization of the dendritic cells in non-Hodgkin's lymphoma, the expressions of adhesion molecules, costimulatory molecules, chemokine receptors and activation markers were assessed. Interestingly, a significantly decreased expression of CD62L and CCR7, receptors necessary for homing to lymph nodes, was identified in dendritic cells in non-Hodgkin's lymphoma, potentially explaining the lack of these cells. Taken together, dendritic cells are phenotypically altered and reduced in number in NHL, potentially contributing to the loss of tumor control in these patients.

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“…Prognostic factors of MALT type lymphoma after eradication of HP infection are reported to be an assessment of deep submucosal invasion by endosonography [43], monoclonal B-cell population [5], t(11;18)(q21;q21) translocation [39,44], alteration of p53 gene [22] and CagA+ strains of H. pylori [9,10]. Recently, expression of MUC-1 mucin and its disappearance in GC in MALT type gBL was reported in follicular DC in the reactive lymphoid hyperplasia [55], suggesting that the disappearance of MUC-1 mucin in follicular DC in MALT predicts occurrence of MALT type gBL. This study suggested that iNOS expression in the GC with lymphoma cell colonization and in the glandular epithelial cells is also a prognostic factor.…”

Section: Discussionmentioning

confidence: 99%