PMID- 18257895
OWN - NLM
STAT- MEDLINE
DCOM- 20080502
LR  - 20111117
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 71
IP  - 3
DP  - 2008 Mar
TI  - HLA-G protein expression as a potential immune escape mechanism in classical 
      Hodgkin's lymphoma.
PG  - 219-26
LID - 10.1111/j.1399-0039.2008.01005.x [doi]
AB  - Classical Hodgkin's lymphoma (cHL) is characterized by the presence of an 
      abundant reactive infiltrate, lacking effective cytotoxic responses. Especially 
      in Epstein-Barr virus (EBV)-negative cHL, the neoplastic Hodgkin-Reed-Sternberg 
      (HRS) cells have lost protein expression of major histocompatibility complex 
      (MHC) class I, enabling escape from cytotoxic T lymphocyte (CTL) responses. 
      However, downregulation of MHC class I generally induces natural killer (NK) cell 
      activation. The paucity of NK cells in the reactive infiltrate of cHL and the 
      systemic NK cell deficiency observed in cHL patients led us to investigate the 
      expression of human leukocyte antigen (HLA)-G, which is known to inhibit NK-cell- 
      and CTL-mediated cytotoxicity. By immunohistochemistry, HLA-G protein was 
      expressed by HRS cells in 54% (95/175) of cHL cases. This expression was 
      associated with absence of MHC class I on the cell surface of HRS cells (P < 
      0.001) and EBV-negative status (P < 0.001). Previously, genetic markers located 
      in the proximity of the HLA-A and HLA-G genes had been shown to be associated 
      with susceptibility to EBV-positive cHL. In the present study, these markers 
      associated with MHC class I protein expression but not with presence of HLA-G. 
      Our results suggest that induction of HLA-G protein expression in HRS cells 
      contributes to the modulation of immune responses observed in cHL.
FAU - Diepstra, A
AU  - Diepstra A
AD  - Department of Pathology, University Medical Center Groningen, University of 
      Groningen, Groningen, The Netherlands. a.diepstra@path.umcg.nl
FAU - Poppema, S
AU  - Poppema S
FAU - Boot, M
AU  - Boot M
FAU - Visser, L
AU  - Visser L
FAU - Nolte, I M
AU  - Nolte IM
FAU - Niens, M
AU  - Niens M
FAU - Te Meerman, G J
AU  - Te Meerman GJ
FAU - van den Berg, A
AU  - van den Berg A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (Genetic Markers)
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-A Antigens)
RN  - 0 (HLA-G Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Child
MH  - Female
MH  - Genetic Markers
MH  - Genotype
MH  - HLA Antigens/genetics/*metabolism
MH  - HLA-A Antigens/genetics
MH  - HLA-G Antigens
MH  - Herpesvirus 4, Human/isolation & purification
MH  - Histocompatibility Antigens Class I/genetics/*metabolism
MH  - Hodgkin Disease/genetics/*immunology/virology
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Reed-Sternberg Cells/immunology/virology
EDAT- 2008/02/09 09:00
MHDA- 2008/05/03 09:00
CRDT- 2008/02/09 09:00
PHST- 2008/02/09 09:00 [pubmed]
PHST- 2008/05/03 09:00 [medline]
PHST- 2008/02/09 09:00 [entrez]
AID - TAN1005 [pii]
AID - 10.1111/j.1399-0039.2008.01005.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2008 Mar;71(3):219-26. doi: 10.1111/j.1399-0039.2008.01005.x.