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Abstract
In Argentina, Epstein-Barr virus (EBV) presence is associated with Hodgkin lymphoma (HL) in patients younger than 10 years, suggesting a relationship between low age of EBV infection and HL. Given that HL is derived from germinal centers (GC), our aim was to compare EBV protein expression and microenvironment markers between pediatric HL patients and EBV+GC in children. Methods: EBV presence and immune cell markers were assessed by in situ hybridization and immunohistochemistry (IHC). Results: Viral latency II pattern was proved in all HL patients and in 81.8% of EBV+ tonsillar GCs. LMP1 and LMP2 co-expression were proved in 45.7% HL cases, but only in 7.7% EBV+ GC in pediatric tonsils. An increase in CD4+, IL10, and CD68+ cells was observed in EBV+ GC. In pediatric HL patients, only the mean of IL10+ cells was statistically higher in EBV+ HL. Conclusions: Our findings point us out to suggest that LMP1 expression may be sufficient to drive neoplastic transformation, that an immune regulatory milieu counteracts cytotoxic environment in EBV-associated Hodgkin lymphoma, and that CD4+ and CD68+ cells may be recruited to act in a local collaborative way to restrict, at least in part, viral-mediated lymphomagenesis in tonsillar GC.
Highlights
The infectious etiology of Hodgkin lymphoma (HL) has been described a long time ago, based on epidemiological evidence that demonstrates a bimodal age-specific incidence pattern that can be observed throughout the western world [1]
A hallmark of HL is the presence of Hodgkin Reed Sternberg (HRS) tumor cells surrounded by various inflammatory immune cells
The aim of this study was to compare Epstein-Barr virus (EBV) viral protein expression and microenvironment composition in pediatric HL samples, a tumor derived from germinal centers (GC) lymphocytes, with normal tonsil
Summary
The infectious etiology of Hodgkin lymphoma (HL) has been described a long time ago, based on epidemiological evidence that demonstrates a bimodal age-specific incidence pattern that can be observed throughout the western world [1]. A hallmark of HL is the presence of Hodgkin Reed Sternberg (HRS) tumor cells surrounded by various inflammatory immune cells. The attraction of inflammatory cells plays an important contribution to the development of HL [2]. The clinical and pathologic features of HL reflect an abnormal immune response, which alters the composition and function of the cells in the surrounding microenvironment and shapes the specific histopathologic appearance of the lymph node. The most abundant cells found in HL are infiltrating CD4+ T cells, which mainly display T helper 2 (Th2) and T regulatory (Treg) phenotypes [3]
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