PMID- 22884899
OWN - NLM
STAT- MEDLINE
DCOM- 20130117
LR  - 20240213
IS  - 1090-2139 (Electronic)
IS  - 0889-1591 (Print)
IS  - 0889-1591 (Linking)
VI  - 26
IP  - 7
DP  - 2012 Oct
TI  - Activating killer-cell immunoglobulin-like receptors (KIR) and their cognate HLA 
      ligands are significantly increased in autism.
PG  - 1122-7
LID - 10.1016/j.bbi.2012.07.014 [doi]
AB  - Killer-cell immunoglobulin-like receptor (KIR) proteins are expressed on natural 
      killer (NK) cells and appear important in innate and adaptive immunity. There are 
      about 14 KIR genes on chromosome 19q13.4, composed of those that inhibit and 
      those that activate NK cell killing. Haplotypes have different combinations of 
      these genes meaning that not all genes are present in a subject. There are two 
      main classes of cognate human leukocyte antigen (HLA) ligands (HLA-Bw4 and 
      HLA-C1/C2) that bind to the inhibitory/activating receptors. As a general rule, 
      the inhibitory state is maintained except when virally infected or tumor cells 
      are encountered; however, both increased activation and inhibition states have 
      been associated with susceptibility and protection against numerous disease 
      states including cancer, arthritis, and psoriasis. Utilizing DNA from 158 
      Caucasian subjects with autism and 176 KIR control subjects we show for the first 
      time a highly significant increase in four activating KIR genes (2DS5, 3DS1, 2DS1 
      and 2DS4) as measured by chi square values and odds ratios. In addition, our data 
      suggests a highly significant increase in the activating KIR gene 2DS1 and its 
      cognate HLA-C2 ligand (2DS1+C2; p = 0.00003 [Odds ratio = 2.87]). This 
      information ties together two major immune gene complexes, the human leukocyte 
      complex and the leukocyte receptor complex, and may partially explain immune 
      abnormalities observed in many subjects with autism.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Torres, Anthony R
AU  - Torres AR
AD  - Center for Persons with Disabilities, Utah State University, Logan, UT 
      84322-6804, USA. Anthony.Torres@usu.edu
FAU - Westover, Jonna B
AU  - Westover JB
FAU - Gibbons, Cole
AU  - Gibbons C
FAU - Johnson, Randall C
AU  - Johnson RC
FAU - Ward, David C
AU  - Ward DC
LA  - eng
GR  - R01 ES016669/ES/NIEHS NIH HHS/United States
GR  - ImNIH/Intramural NIH HHS/United States
GR  - HHSN261200800001C/RC/CCR NIH HHS/United States
GR  - HHSN261200800001E/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120803
PL  - Netherlands
TA  - Brain Behav Immun
JT  - Brain, behavior, and immunity
JID - 8800478
RN  - 0 (HLA Antigens)
RN  - 0 (Receptors, KIR)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Autistic Disorder/genetics/*immunology
MH  - Cohort Studies
MH  - DNA/genetics
MH  - Female
MH  - Gene Frequency
MH  - Genotype
MH  - HLA Antigens/genetics/*immunology
MH  - Humans
MH  - Killer Cells, Natural/metabolism
MH  - Male
MH  - Odds Ratio
MH  - Polymerase Chain Reaction
MH  - Receptors, KIR/genetics/*immunology
PMC - PMC3469320
MID - NIHMS404038
COIS- Conflict of Interest Statement: All authors declare that there are no conflicts 
      of interest.
EDAT- 2012/08/14 06:00
MHDA- 2013/01/18 06:00
PMCR- 2013/10/01
CRDT- 2012/08/14 06:00
PHST- 2012/04/09 00:00 [received]
PHST- 2012/07/16 00:00 [revised]
PHST- 2012/07/19 00:00 [accepted]
PHST- 2012/08/14 06:00 [entrez]
PHST- 2012/08/14 06:00 [pubmed]
PHST- 2013/01/18 06:00 [medline]
PHST- 2013/10/01 00:00 [pmc-release]
AID - S0889-1591(12)00197-3 [pii]
AID - 10.1016/j.bbi.2012.07.014 [doi]
PST - ppublish
SO  - Brain Behav Immun. 2012 Oct;26(7):1122-7. doi: 10.1016/j.bbi.2012.07.014. Epub 
      2012 Aug 3.