Non Classical HLA Genes and Non-HLA Genes in a Population of Infants at Familial Risk of Atopy

نویسندگان

  • A. De Silvestri
  • C. Belloni
  • M. De Amici
  • P. Mazzola
  • M. Zorzetto
  • M. Martinetti
  • L. Salvaneschi
  • M. Cuccia
چکیده

AIM We investigated on parental history and IgE serum level in 2588 consecutive newborns to individuate babies "at risk" of atopy at birth and we analysed the polymorphisms of class III region to evaluate the association with immunogenetic markers of HLA: C4A, C4B, LTA, RAGE and TNFA genes; we performed TNF and IgE receptor (FCERB1) physiologically related gene polymorphisms. RESULT 791 babies/2588 (30.6%) were considered "at risk" for atopy and followed-up: 400 had familial history of atopy (at least one parent or sibling), 256 had IgE >0.35 kUA/l at birth and during the follow-up and 135 were positive for both conditions. The allele C4B2 was significantly more frequent in the sample of babies at risk (22.1% vs 10%, p< 0.001). Furthermore, the mean value of IgE at birth in babies carrying the allele C4B2 was 2.26 KUA/l versus 0.74 KUA/l in those not carrying this allele (p=0.01). No significant association emerged for RAGE at the centromeric end of class III region and for LTA, TNFA at the telomeric one. TNFRI, TNFRII and FCERB1 gene polymorphisms also seemed not implicated. CONCLUSION Our study confirms that HLA class III region seems involved in familial predisposition to atopy, and C4B gene probably acts as a marker of a more restricted subregion.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Frequencies of HLA-E*01:01/*01:03 Alleles in an Iranian Healthy Population and Its Comparison with Hyperglycemia Patients

Background and Aims: The human leukocyte antigen-E (HLA-E) is a member of non-classical HLA class-I genes which is highly conserved through evolution. In general, so far 25 alleles of HLA-E have been described. However, the existence of only two allelic group; HLA-E*01:01 and HLA-E*01:03 have been demonstrated in all the populations. HLA-E*01:01 and HLA-E*01:03 differ only at codon 107 of exon ...

متن کامل

مقایسه آنالیز ژنوتیپی KIR/HLA در جمعیت‌های لر و ایرانی

Introduction: Killer-cell Immunoglobulin-like Receptors (KIR) are the members of inhibitory and activating receptors expressed chiefly by the natural killer cells (NK). KIR proteins operate as receptors detecting human leukocyte antigen class Ι molecules (HLA). KIRs and their class Ι HLA ligands contribute in the pathogenesis of many kinds of diseases. The aim of this study was to genotypic ana...

متن کامل

P 70: Primary Progressive MS and Affecting Genes

Multiple sclerosis is a CNS autoimmune disease configured by demyelination, inflammation, and degeneration of axons. This disease inflict great harms to patients. The most common problem is inability to control musculoskeletal system and decrease in mobility. These consequences could vary from patients to patients. About 10-15% of all MS patients develop primary progressive MS (PPMS). Despite t...

متن کامل

P-145: Role of Human Leukocyte Antigen in Miscarriage

Background: During pregnancy, the maternal immune system is in close contact with cells and tissue from the semiallogenic fetus .The human leucocyte antigen (HLA) class Ib molecules, HLA-E, -F and -G, are expressed at the materno-fetal interface. Because of the apparent immunoregulatory functions of these proteins, they may be involved in successful acceptance of the semi-allogenic fetus during...

متن کامل

P-164: Human Leukocyte Antigen Class Ib and Pregnancy Success

Background: During pregnancy, the maternal immune system is in close contact with cells and tissue from the semiallogenic fetus .The Human Leucocyte Antigen (HLA) class Ib molecules, HLA-E, -F and -G, are expressed at the materno-fetal interface. Because of the apparent immunoregulatory functions of these proteins, they may be involved in successful acceptance of the semi-allogenic fetus during...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 22  شماره 

صفحات  -

تاریخ انتشار 2006