Immune escape mechanisms in Hodgkin's disease

Citation
S. Poppema et al., Immune escape mechanisms in Hodgkin's disease, ANN ONCOL, 9, 1998, pp. 21-24
Citations number
44
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Oncology,"Onconogenesis & Cancer Research
Journal title
ANNALS OF ONCOLOGY
ISSN journal
0923-7534 → ACNP
Volume
9
Year of publication
1998
Supplement
5
Pages
21 - 24
Database
ISI
SICI code
0923-7534(1998)9:<21:IEMIHD>2.0.ZU;2-E
Abstract
Background: The nodular sclerosis and mixed cellularity subtypes of Hodgkin 's disease are histologically characterised by a small population of neopla stic cells, the so-called Reed-Sternberg cells and their mononuclear varian ts (RS cells) and an extensive admixture of other cell types including lymp hocytes, plasma cells, eosinophils, and histiocytes. The nature of this inf iltrate is largely known, but the mechanisms and functional effects are not . The small lymphocytes immediately surrounding the RS cells are mostly CD4 + T cells that express early activation markers. The absence of prominent s pecific cytotoxic I cell or natural killer (NK) cell populations seems to a rgue against a Th1-type response, whereas the sometimes prominent admixture of plasma cells and eosinophils is suggestive of a Th2-type response. Enri chment of the CD4 T-cell population may result from selective influx of CD4 T cells or from selective depletion of CD8 cells and NK cells. Results and discussion: The T cells surrounding RS cells have an immuno-phe notype and cytokine production capability consistent with a Th2-type respon se. RS cells express several members of the TNF receptor family such as the FAS ligand (CD95L) that may induce apoptosis of activated, FAS expressing, CD8+ T cells and NK cells. The RS cells also produce TGF beta and interleu kin-10 that may downmodulate the Th1 response. In addition, the Reed-Sternb erg cells produce the chemokine TARC that could lead to the specific attrac tion of a Th2 I-cell subset. Conclusion: RS cells have several mechanisms that may allow it to escape an effective immune response. The relative contributions of each of these and other potential mechanisms are not yet known.