PMID- 10658979
OWN - NLM
STAT- MEDLINE
DCOM- 20000302
LR  - 20201215
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 61
IP  - 1
DP  - 2000 Jan
TI  - The HLA crossroad in tumor immunology.
PG  - 65-73
AB  - It is generally accepted that human and experimental tumor cells can lose major 
      histocompatibility complex (MHC) class I molecules. These human leukocyte antigen 
      (HLA) losses are detected when the primary tumor breaks the basal membrane, 
      invades the surrounding tissues, and starts to metastasize. These altered HLA 
      class I phenotypes probably constitute the major tumor escape mechanism facing 
      anti-tumor T-cell mediated responses. Thus, it is important to characterize these 
      phenotypes in clinical tumor samples, analyze the mechanism(s) responsible for 
      them, and counsel patients before and during peptide anti-cancer immunotherapy. 
      The present paper summarizes the most relevant altered HLA class I phenotypes 
      found in human tumor samples, indicates their frequency, and outlines the 
      mechanisms implicated. This review also points out that the natural killer (NK) 
      escape mechanism of HLA class I deficient cancer cells is yet to be defined. 
      Knowledge accumulated to date reveals that HLA class I molecules are an important 
      crossroad in tumor immunology.
FAU - Algarra, I
AU  - Algarra I
AD  - Departamento de Ciencias de la Salud, Facultad de Ciencias Experimentales, 
      Universidad de Jaen, Spain.
FAU - Cabrera, T
AU  - Cabrera T
FAU - Garrido, F
AU  - Garrido F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Histocompatibility Antigens Class I)
SB  - IM
MH  - Histocompatibility Antigens Class I/*metabolism
MH  - Humans
MH  - Immunotherapy
MH  - Killer Cells, Natural/immunology
MH  - Neoplasms/*immunology/therapy
MH  - Phenotype
MH  - T-Lymphocytes/immunology
MH  - Tumor Escape
RF  - 41
EDAT- 2000/02/05 09:00
MHDA- 2000/03/04 09:00
CRDT- 2000/02/05 09:00
PHST- 2000/02/05 09:00 [pubmed]
PHST- 2000/03/04 09:00 [medline]
PHST- 2000/02/05 09:00 [entrez]
AID - S0198-8859(99)00156-1 [pii]
AID - 10.1016/s0198-8859(99)00156-1 [doi]
PST - ppublish
SO  - Hum Immunol. 2000 Jan;61(1):65-73. doi: 10.1016/s0198-8859(99)00156-1.