PMID- 21274527
OWN - NLM
STAT- MEDLINE
DCOM- 20110617
LR  - 20211020
IS  - 1432-1211 (Electronic)
IS  - 0093-7711 (Print)
IS  - 0093-7711 (Linking)
VI  - 63
IP  - 5
DP  - 2011 May
TI  - Functional analysis of frequently expressed Chinese rhesus macaque MHC class I 
      molecules Mamu-A1*02601 and Mamu-B*08301 reveals HLA-A2 and HLA-A3 supertypic 
      specificities.
PG  - 275-90
LID - 10.1007/s00251-010-0502-8 [doi]
AB  - The Simian immunodeficiency virus (SIV)-infected Indian rhesus macaque (Macaca 
      mulatta) is the most established model of HIV infection and AIDS-related 
      research, despite the potential that macaques of Chinese origin is a more 
      relevant model. Ongoing efforts to further characterize the Chinese rhesus 
      macaques' major histocompatibility complex (MHC) for composition and function 
      should facilitate greater utilization of the species. Previous studies have 
      demonstrated that Chinese-origin M. mulatta (Mamu) class I alleles are more 
      polymorphic than their Indian counterparts, perhaps inferring a model more 
      representative of human MHC, human leukocyte antigen (HLA). Furthermore, the 
      Chinese rhesus macaque class I allele Mamu-A1*02201, the most frequent allele 
      thus far identified, has recently been characterized and shown to be an HLA-B7 
      supertype analog, the most frequent supertype in human populations. In this 
      study, we have characterized two additional alleles expressed with high frequency 
      in Chinese rhesus macaques, Mamu-A1*02601 and Mamu-B*08301. Upon the development 
      of MHC-peptide-binding assays and definition of their associated motifs, we 
      reveal that these Mamu alleles share peptide-binding characteristics with the 
      HLA-A2 and HLA-A3 supertypes, respectively, the next most frequent human 
      supertypes after HLA-B7. These data suggest that Chinese rhesus macaques may 
      indeed be a more representative model of HLA gene diversity and function as 
      compared to the species of Indian origin and therefore a better model for 
      investigating human immune responses.
FAU - Southwood, Scott
AU  - Southwood S
AD  - Department of Vaccine Discovery, La Jolla Institute for Allergy and Immunology, 
      La Jolla, CA 92037, USA.
FAU - Solomon, Christopher
AU  - Solomon C
FAU - Hoof, Ilka
AU  - Hoof I
FAU - Rudersdorf, Richard
AU  - Rudersdorf R
FAU - Sidney, John
AU  - Sidney J
FAU - Peters, Bjoern
AU  - Peters B
FAU - Wahl, Angela
AU  - Wahl A
FAU - Hawkins, Oriana
AU  - Hawkins O
FAU - Hildebrand, William
AU  - Hildebrand W
FAU - Mothe, Bianca R
AU  - Mothe BR
FAU - Sette, Alessandro
AU  - Sette A
LA  - eng
GR  - R01 AI070902/AI/NIAID NIH HHS/United States
GR  - R15 AI064175/AI/NIAID NIH HHS/United States
GR  - R01 AI070902-01A2/AI/NIAID NIH HHS/United States
GR  - R15 AI064175-01/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110128
PL  - United States
TA  - Immunogenetics
JT  - Immunogenetics
JID - 0420404
RN  - 0 (HLA-A2 Antigen)
RN  - 0 (HLA-A3 Antigen)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Mamu-A 01 antigen)
RN  - 0 (Mamu-B 01 antigen, Macaca mulatta)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Base Sequence
MH  - Cells, Cultured
MH  - *Disease Models, Animal
MH  - Gene Frequency
MH  - HLA-A2 Antigen/genetics/immunology
MH  - HLA-A3 Antigen/genetics/immunology
MH  - Histocompatibility Antigens Class I/genetics/*immunology
MH  - Macaca mulatta/genetics/*immunology
MH  - Molecular Sequence Data
MH  - Simian Immunodeficiency Virus/genetics/immunology
PMC - PMC3068250
EDAT- 2011/01/29 06:00
MHDA- 2011/06/18 06:00
PMCR- 2011/01/28
CRDT- 2011/01/29 06:00
PHST- 2010/09/28 00:00 [received]
PHST- 2010/12/07 00:00 [accepted]
PHST- 2011/01/29 06:00 [entrez]
PHST- 2011/01/29 06:00 [pubmed]
PHST- 2011/06/18 06:00 [medline]
PHST- 2011/01/28 00:00 [pmc-release]
AID - 502 [pii]
AID - 10.1007/s00251-010-0502-8 [doi]
PST - ppublish
SO  - Immunogenetics. 2011 May;63(5):275-90. doi: 10.1007/s00251-010-0502-8. Epub 2011 
      Jan 28.