Association of polymorphisms of IGF1R and genes in the transforming growth factor-β bone morphogenetic protein pathway with Bacteremia in sickle cell anemia

被引：33
作者：
Adewoye, Adeboye H.
Nolan, Vikki G.
Ma, Qianli
Baldwin, Clinton
Wyszynski, Diego F.
Farrell, John J.
Farrer, Lindsay A.
Steinberg, Martin H.
机构：
[1] Boston Univ, Sch Med, Dept Med, Boston, MA 02215 USA
[2] Boston Univ, Sch Med, Dept Pediat, Boston, MA 02215 USA
[3] Boston Univ, Sch Med, Ctr Human Genet, Boston, MA 02215 USA
来源：
CLINICAL INFECTIOUS DISEASES | 2006年 / 43卷 / 05期
关键词：
D O I：
10.1086/506356
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Infection and bacteremia are common in sickle cell disease. We hypothesized that, consistent with evidence for the genetic modulation of other disease complications, the risk of developing bacteremia might also be genetically modulated. Accordingly, we studied the association of single nucleotide polymorphisms (SNPs) in candidate genes with the risk of bacteremia in sickle cell anemia. We found significant associations with SNPs in IGF1R and genes of the TGF-beta/BMP pathway (BMP6, TGFBR3, BMPR1A, SMAD6 and SMAD3). We suggest that both IGF1R and the TGF-beta/BMP pathway could play important roles in immune function in sickle cell anemia and their polymorphisms may help identify a "bacteremia-prone" phenotype.
引用
收藏
页码：593 / 598
页数：6
相关论文
共 34 条
  • [1] Ashley-Koch AE, 2005, BLOOD, V106, p26A
  • [2] Association of klotho, bone morphogenic protein 6, and annexin A2 polymorphisms with sickle cell osteonecrosis
    Baldwin, C
    Nolan, VG
    Wyszynski, DF
    Ma, QL
    Sebastiani, P
    Embury, SH
    Bisbee, A
    Farrell, J
    Farrer, L
    Steinberg, MH
    [J]. BLOOD, 2005, 106 (01) : 372 - 375
  • [3] Insulin-like growth factor-1 controls type 2 T cell-independent B cell response
    Baudler, S
    Baumgartl, J
    Hampel, B
    Buch, T
    Waisman, A
    Snapper, CM
    Krone, W
    Brüning, JC
    [J]. JOURNAL OF IMMUNOLOGY, 2005, 174 (09) : 5516 - 5525
  • [4] Genetics and genomics in infectious disease susceptibility
    Blackwell, JM
    [J]. TRENDS IN MOLECULAR MEDICINE, 2001, 7 (11) : 521 - 526
  • [5] Mechanisms of disease:: Role of transforming growth factor β in human disease.
    Blobe, GC
    Schiemann, WP
    Lodish, HF
    [J]. NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) : 1350 - 1358
  • [6] Intracellular demonstration of active TGF beta 1 in B cells and plasma cells of autoimmune mice - IgG-Bound TGF beta 1 suppresses neutrophil function and host defense against Staphylococcus aureus infection
    Caver, TE
    OSullivan, FX
    Gold, LI
    Gresham, HD
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (11) : 2496 - 2506
  • [7] NON-SH2 DOMAINS WITHIN INSULIN-RECEPTOR SUBSTRATE-1 AND SHC MEDIATE THEIR PHOSPHOTYROSINE-DEPENDENT INTERACTION WITH THE NPEY MOTIF OF THE INSULIN-LIKE GROWTH-FACTOR-I RECEPTOR
    CRAPARO, A
    ONEILL, TJ
    GUSTAFSON, TA
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (26) : 15639 - 15643
  • [8] Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
    Datta, SR
    Dudek, H
    Tao, X
    Masters, S
    Fu, HA
    Gotoh, Y
    Greenberg, ME
    [J]. CELL, 1997, 91 (02) : 231 - 241
  • [9] Smad-dependent and Smad-independent pathways in TGF-β family signalling
    Derynck, R
    Zhang, YE
    [J]. NATURE, 2003, 425 (6958) : 577 - 584
  • [10] Evidence for the direct interaction of the insulin-like growth factor I receptor with IRS-1, Shc, and Grb10
    Dey, BR
    Frick, K
    Lopaczynski, W
    Nissley, SP
    Furlanetto, RW
    [J]. MOLECULAR ENDOCRINOLOGY, 1996, 10 (06) : 631 - 641
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