PMID- 11872237
OWN - NLM
STAT- MEDLINE
DCOM- 20020809
LR  - 20220316
IS  - 0198-8859 (Print)
IS  - 0198-8859 (Linking)
VI  - 63
IP  - 3
DP  - 2002 Mar
TI  - Infectious complications in sickle cell disease are influenced by HLA class II 
      alleles.
PG  - 194-9
AB  - Despite systematic antibiotic therapy, severe infections (septicemia, meningitis, 
      or osteomyelitis) are a major cause of mortality and morbidity in children with 
      sickle cell disease (SCD). In this study, we explored the possibility that 
      polymorphism at the human leukocyte antigen (HLA) locus might constitute an 
      immunogenetic modifying factor to the intrinsic susceptibility to infection in 
      patients with SCD. A cohort of 80 SCD patients living in Paris, 43 with at least 
      one major infectious complication and 37 without infections, were typed for HLA 
      class II loci by polymerase chain reaction-sequence-specific primers (PCR-SSP). 
      We found that significantly more patients without infections carry the HLA class 
      II DRB1*15 specificity than did patients with infections (21.6% in the first 
      group, versus 4.7% in the second group; chi(2) = 10.47, p(c) = 0.01), supporting 
      a protective effect of this allele. Conversely, significantly more patients were 
      found to carry the DQB1*03 specificity within the group of severe infections, 
      supporting a negative effect (34.9% versus 12.2%, chi(2) = 9.41, p(c) = 0.01). 
      These findings suggest a direct involvement of HLA polymorphism in the 
      development of major infections in SCD. Together with previous data on 
      polymorphism of the Fc receptor and of the mannose-binding lectin, they provide 
      evidence for a polygenic immunomodulation of the constitutively increased 
      infectious risk in SCD.
FAU - Tamouza, Ryad
AU  - Tamouza R
AD  - Laboratoire d'Immunologie et d'Histocompatibilite, AP-HP, IUH, and INSERM U396, 
      Hopital Saint-Louis, Paris, France. tamouza@histo.chu-stlouis.fr
FAU - Neonato, Maria Grazia
AU  - Neonato MG
FAU - Busson, Marc
AU  - Busson M
FAU - Marzais, Francois
AU  - Marzais F
FAU - Girot, Robert
AU  - Girot R
FAU - Labie, Dominique
AU  - Labie D
FAU - Elion, Jacques
AU  - Elion J
FAU - Charron, Dominique
AU  - Charron D
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 (HLA-D Antigens)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ beta-Chains)
RN  - 0 (HLA-DQB1 antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
SB  - IM
MH  - Adolescent
MH  - Anemia, Sickle Cell/*complications/*genetics
MH  - Bacteremia/pathology
MH  - Bacterial Infections/*complications
MH  - Child
MH  - Female
MH  - Gene Frequency
MH  - Genetic Predisposition to Disease
MH  - HLA-D Antigens/*genetics
MH  - HLA-DQ Antigens/genetics/metabolism
MH  - HLA-DQ beta-Chains
MH  - HLA-DR Antigens/genetics/metabolism
MH  - HLA-DRB1 Chains
MH  - Humans
MH  - Male
MH  - Meningitis/microbiology/pathology
MH  - Osteomyelitis/microbiology/pathology
MH  - Pneumococcal Infections/complications
MH  - *Polymorphism, Genetic/genetics
MH  - Salmonella Infections/complications
MH  - Staphylococcal Infections/complications
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 - S0198885901003780 [pii]
AID - 10.1016/s0198-8859(01)00378-0 [doi]
PST - ppublish
SO  - Hum Immunol. 2002 Mar;63(3):194-9. doi: 10.1016/s0198-8859(01)00378-0.