PMID- 3059799
OWN - NLM
STAT- MEDLINE
DCOM- 19890125
LR  - 20190626
IS  - 0002-9343 (Print)
IS  - 0002-9343 (Linking)
VI  - 85
IP  - 6A
DP  - 1988 Dec 23
TI  - Diversity and regulation of expression of human leukocyte antigen class II 
      molecules.
PG  - 6-8
AB  - The initiation of an immune response requires that a foreign antigen be degraded, 
      and that one of the degradative fragments be presented in the context of a human 
      leukocyte antigen (HLA) class II molecule to an antigen-specific helper T cell. 
      The success of this process is maximized by the diversity of the class II 
      molecules possessed by a given person. The expression of the HLA class II 
      molecules is highly selective. Aberrant expression has been postulated to be 
      responsible for autoimmune disease. The interaction of inducible tissue-specific 
      transacting factors with cis-acting genetic elements adjacent to the coding 
      portion of the class II genes is responsible for both normal and aberrant 
      expression of class II molecules. The cDNA encoding one such transacting factor 
      that binds to the cis-acting element known as the Y box has been cloned.
FAU - Schwartz, B D
AU  - Schwartz BD
AD  - Howard Hughes Medical Institute Laboratories, Washington University School of 
      Medicine, St. Louis, Missouri 63110.
LA  - eng
GR  - 18925/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Am J Med
JT  - The American journal of medicine
JID - 0267200
RN  - 0 (HLA-D Antigens)
RN  - 0 (HLA-DP Antigens)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DR Antigens)
SB  - IM
MH  - *Gene Expression Regulation
MH  - HLA-D Antigens/biosynthesis/*genetics
MH  - HLA-DP Antigens/genetics
MH  - HLA-DQ Antigens/genetics
MH  - HLA-DR Antigens/genetics
MH  - Humans
RF  - 12
EDAT- 1988/12/23 00:00
MHDA- 1988/12/23 00:01
CRDT- 1988/12/23 00:00
PHST- 1988/12/23 00:00 [pubmed]
PHST- 1988/12/23 00:01 [medline]
PHST- 1988/12/23 00:00 [entrez]
AID - 0002-9343(88)90370-1 [pii]
AID - 10.1016/0002-9343(88)90370-1 [doi]
PST - ppublish
SO  - Am J Med. 1988 Dec 23;85(6A):6-8. doi: 10.1016/0002-9343(88)90370-1.