Common polymorphisms and alternative splicing in the ILT3 gene are not associated with atopy

Abstract

Recently, a linkage of the chromosomal region 19q13.4 with bronchial asthma has been demonstrated. This region harbours the so-called leucocyte receptor cluster with the gene for immunoglobulin-like-transcript 3 (ILT3) as a member. ILT3 represents an inhibitory receptor bearing three immunoreceptor tyrosine inhibitory motifs (ITIM). The protein mediates downregulation of cell activation through recruitment of different SH2-containing protein tyrosine phosphatases. With regard to the negative immunoregulatory function particularly on B-cells, ILT3 represents a candidate gene for atopy and asthma. The aim of this study was to screen for common polymorphisms in the gene coding for ILT3 and to test for association with the atopic phenotype. Using single-stranded conformal polymorphism-analysis and direct genomic sequencing seven polymorphisms, three mutations, a common deletion of 7 bp in the third intron and evidence for further alternative splicing of the ILT3 gene were found. Although no association was found with atopy phenotypes, it might prove useful to test for association with bronchial asthma.

Inhibitory Immunoglobulin-Like Receptors LILRB and PIR-B Negatively Regulate Osteoclast Development

“…On the other hand, LILRB4 polymorphisms have been screened for their possible association with atopy, but no apparent association was detected (46). The association of either LILRB3 or LILRB4 with bone disorders, such as rheumatoid arthritis or bone metabolic diseases, including osteopetrosis and osteoporosis, has not been reported so far.…”

Long-term persistence of both functional and non-functional alleles at the leukocyte immunoglobulin-like receptor A3 (LILRA3) locus suggests balancing selection

“…Both LILRB1 and LILRB2 bind to a broad range of classical and nonclassical HLA class I molecules, as well as UL18 (MHC class I homologue of human cytomegalovirus). A number of variations have been identified in LILR genes (Heinzmann et al 2000;Kuroki et al 2005;Norman et al 2003;Papanikolaou et al 2004;Torkar et al 2000;Wilson et al 2000), and some polymorphisms of LILR genes are associated with susceptibility to diseases such as rheumatoid arthritis and multiple sclerosis (MS) (Koch et al 2005;Kuroki et al 2005). A murine homologue of LILR has been proposed to be the paired Ig-like receptor (PIR), which also consists of activating (PIR-A) and inhibitory (PIR-B) forms.…”

Interaction of T-cell and antigen presenting cell co-stimulatory genes in childhood IgE

“…Herein, we confirm the main effects of the genes CD86, CD40 and ICOS with respect to serum IgE levels. In addition, we showed that LILRB4, which did not appear to have a main effect on IgE levels in single gene association studies [5,27], does affect IgE levels in interaction with other gene polymorphisms. Although we did not find main effects for CTLA4, HLA-G and PDCD1, our results are not in contradiction with previous studies because the associated atopic phenotypes were different, e.g.…”

“…CD86 [3], CD40 [4], CTLA4 [5,26], HLA-G [6], ICOS [7] and PDCD1 [8], yet other genes were found not to be associated with atopy such as CD28 [5] and LILRB4 [27]. A summary of these association studies is presented in table E4 of the supplementary material.…”