PMID- 11872238
OWN - NLM
STAT- MEDLINE
DCOM- 20020809
LR  - 20190906
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 63
IP  - 3
DP  - 2002 Mar
TI  - Loss or downregulation of HLA class I expression at the allelic level in acute 
      leukemia is infrequent but functionally relevant, and can be restored by 
      interferon.
PG  - 200-10
AB  - Human leukocyte antigen (HLA) class I expression at the allelic level was 
      analyzed in 397 acute myeloid leukemia (AML) and 186 acute lymphoid leukemia 
      (ALL) using a complement-dependent cytotoxicity assay. Impaired recognition 
      possibly due to HLA downregulation was observed in 2% of the patients with AML 
      and ALL in complete remission, and in 8%-15% in the groups with blasts. In 15 
      instances of diminished cytotoxicity, leukemic cells and control PHA blasts from 
      the same patients were further analyzed using flow cytometry. In 4/6 ALL and 4/9 
      AML patients HLA downregulation or complete loss (2 patients) of cell surface 
      expression could be confirmed. No genomic abnormalities were observed. In 
      addition, 12 AML and 13 ALL patients were tested during relapse using flow 
      cytometry. In 1/12 AML patients and 1/13 ALL patients allelic downregulation of 
      cell surface expression was found. In two patients tested, downregulation or loss 
      of cell surface expression of HLA class I antigens corresponded with impaired T 
      cell mediated lysis by HLA restricted cytotoxic T lymphocyte.Treatment of the 
      cells with alpha- or gamma-interferon could restore HLA class I expression and 
      T-cell recognition. In conclusion, downregulation of cell surface expression of 
      HLA class I expression at the allelic level in AML and ALL is infrequent but 
      functionally relevant. HLA downregulation was reversible and T-cell recognition 
      could be restored by alpha- or gamma-interferon.
FAU - Brouwer, Rolf E
AU  - Brouwer RE
AD  - Laboratory of Experimental Hematology, Department of Hematology, Leiden, The 
      Netherlands.
FAU - van der Heiden, Pim
AU  - van der Heiden P
FAU - Schreuder, Geziena M T
AU  - Schreuder GM
FAU - Mulder, Arend
AU  - Mulder A
FAU - Datema, Gert
AU  - Datema G
FAU - Anholts, Jacqy D H
AU  - Anholts JD
FAU - Willemze, Roel
AU  - Willemze R
FAU - Claas, Frans H J
AU  - Claas FH
FAU - Falkenburg, J H Frederik
AU  - Falkenburg JH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (HLA Antigens)
RN  - 0 (HLA-A Antigens)
RN  - 0 (HLA-B Antigens)
RN  - 0 (Interferon-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Acute Disease
MH  - Adult
MH  - Aged
MH  - Antibodies, Monoclonal
MH  - DNA Mutational Analysis
MH  - Down-Regulation
MH  - Female
MH  - Gene Expression Regulation, Leukemic
MH  - HLA Antigens/*metabolism
MH  - HLA-A Antigens/metabolism
MH  - HLA-B Antigens/metabolism
MH  - Humans
MH  - Interferon-alpha/genetics/pharmacology
MH  - Interferon-gamma/genetics/pharmacology
MH  - Leukemia, Myeloid/*immunology
MH  - Male
MH  - Middle Aged
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*immunology
MH  - T-Lymphocytes, Cytotoxic/immunology
EDAT- 2002/03/02 10:00
MHDA- 2002/08/10 10:01
CRDT- 2002/03/02 10:00
PHST- 2002/03/02 10:00 [pubmed]
PHST- 2002/08/10 10:01 [medline]
PHST- 2002/03/02 10:00 [entrez]
AID - S0198885901003810 [pii]
AID - 10.1016/s0198-8859(01)00381-0 [doi]
PST - ppublish
SO  - Hum Immunol. 2002 Mar;63(3):200-10. doi: 10.1016/s0198-8859(01)00381-0.