Microenvironment abnormalities and lymphomagenesis: Immunological aspects

Taylor, Joan; Gribben, John G.

doi:10.1016/j.semcancer.2015.07.004

Cited by 21 publications

(19 citation statements)

References 127 publications

(146 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies performed in EBV+HL showed a similar increment of immunosuppressive cytokine genes (IL-10 and TGFβ) expression. IL-10 is secreted by HRS cells in HL and also by tumor cells and associated macrophages in BL 36 . In our series, we found that IL-10 is produced both by tumor cells and the reactive microenvironment, as shown by IHC, although no statistically significant difference was detected according to EBV status.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic response against Epstein Barr virus coexists with diffuse large B-cell lymphoma tolerogenic microenvironment: clinical features and survival impact

Cohen

Vistarop

Huaman³

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Epstein–Barr Virus (EBV) is present in neoplastic cells of 15% of Asian and Latin-American diffuse large B-cell lymphoma (DLBCL) patients. Even though a tolerogenic microenvironment was recently described in DLBCL, little is known concerning immunomodulatory features induced by EBV. As suggested in Hodgkin lymphoma, EBV-specific cytotoxic T-cells are increased but showing immune exhaustion features. Hence, host immunity suppression may play a critical role in tumor progression. This study aimed to investigate, whether an association between tumor microenvironment features and EBV presence is taking place, and its clinical correlate. The incidence of EBV+DLBCL NOS was 12.6% in this cohort. Cytokine and chemokine transcripts expression and immunophenotype analysis showed that EBV infection was associated with increased gene expression of immunosuppressive cytokine (IL-10) together with increased CD8+ T-cells and granzyme B+ cytotoxic effector cells. However, this specific response coexists with a tolerogenic milieu, by PD-1 expression, in EBV+ and EBV−DLBCL cases. High PD-1+ cell counts, EBV presence and low CCL22 expression were associated with worse survival, supporting our hypothesis that EBV-specific response is mounted locally and its inhibition by, for example PD-1+ cells, may negatively affect outcome. The better understanding of the interplay between lymphoma cells and microenvironment in a viral framework could thereby facilitate the discovery of new targets for innovative anti-lymphoma treatment strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

Cytotoxic response against Epstein Barr virus coexists with diffuse large B-cell lymphoma tolerogenic microenvironment: clinical features and survival impact

Cohen

Vistarop

Huaman³

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…The presence of natural killer cells (NK cells) and natural killer T cells in the majority of solid tumors often means a good prognosis [1]. Within the TME, NK cells and CTLs are capable of recognizing malignant cells owing to the expression of NKG2D and T cell receptors, respectively [45]. Monocytes are recruited from the circulation and differentiate into macrophages within the TME where stromal and tumor cells provide chemokines and growth factors mainly CCL2, CSF1, CCL18, CCL20, CXCL12, and VEGF-A [46].…”

Section: Cells Of the Adaptive Immune System In Tmementioning

confidence: 99%

Role of Mast Cells in Shaping the Tumor Microenvironment

Komi

Redegeld

2019

Clinic Rev Allerg Immunol

254

181

View full text Add to dashboard Cite

Early mast cell (MC) infiltration has been reported in a wide range of human and animal tumors particularly malignant melanoma and breast and colorectal cancer. The consequences of their presence in the tumor microenvironment (TME) or at their margins still remain unclear as it is associated with a good or poor prognosis based on the type and anatomical site of the tumor. Within the tumor, MC interactions occur with infiltrated immune cells, tumor cells, and extracellular matrix (ECM) through direct cell-tocell interactions or release of a broad range of mediators capable of remodeling the TME. MCs actively contribute to angiogenesis and induce neovascularization by releasing the classical proangiogenic factors including VEGF, FGF-2, PDGF, and IL-6, and nonclassical proangiogenic factors mainly proteases including tryptase and chymase. MCs support tumor invasiveness by releasing a broad range of matrix metalloproteinases (MMPs). MC presence within the tumor gained additional significance when it was assumed that controlling its activation by tyrosine kinase inhibitors (imatinib and masitinib) and tryptase inhibitors (gabexate and nafamostat mesylate) or controlling their interactions with other cell types may have therapeutic benefit.

show abstract

“…they reduce secretion of proinflammatory IFN-g and TNF-a by Th 1 cells and of IL-17 by Th 17 cells. Such ac-tivities promote carcinogenesis via inhibiting secretion of antitumor mediators [33]. TGF-b is a cytokine that inhibits excessive proliferation and repressor genes encoding for cytotoxic mediators, including perforin, granzymes A and B and IFN-g [34].…”

Section: Immune Response Modulation By H Pylorimentioning

confidence: 99%

“…This happens until carcinogenic cells become resistant to the stimuli initiated by this mediator, for example by the increased activity of mammalian target of rapamycin (mTOR), which makes carcinogenic cells insensitive to TGF-b-mediated antiproliferative activity [35]. In such situations, elevated TGF-b level is beneficial for lymphoma development because it disrupts cytotoxic and proapoptotic activity to tumor-altered cells [33]. In an in vivo mouse model, Craig et al demonstrated the ability of Helicobacter spp.…”

Section: Immune Response Modulation By H Pylorimentioning

confidence: 99%