Association study between interleukin-12 receptor beta 1/ beta 2 genes and type 1 diabetes or asthma in the Japanese population

Interleukin-12 (IL-12) secreted from macrophages or dendritic cells plays an important role in the protection against intracellular pathogens as well as the developmental commitment of T helper 1 cells. IL-12 exerts its biological effects through binding to specific IL-12 receptors (IL-12Rs) termed...

Full description

Saved in:
Bibliographic Details
Published inImmunogenetics (New York) Vol. 55; no. 3; pp. 189 - 192
Main Authors Bassuny, WM, Ihara, K, Kimura, J, Ichikawa, S, Kuromaru, R, Miyako, K, Kusuhara, K, Sasaki, Y, Kohno, H, Matsuura, N, Nishima, S, Hara, T
Format Journal Article
LanguageEnglish
Published 01.06.2003
Online AccessGet full text

Cover

Loading…
More Information
Summary:Interleukin-12 (IL-12) secreted from macrophages or dendritic cells plays an important role in the protection against intracellular pathogens as well as the developmental commitment of T helper 1 cells. IL-12 exerts its biological effects through binding to specific IL-12 receptors (IL-12Rs) termed IL-12R beta 1 and IL 12R beta 2. In this paper, we performed association studies between the three reported polymorphisms (Q214R, M365T and G378R) of the IL-12R beta 1 gene or the newly identified polymorphisms (P238L, IVS9 -7G>A, IVS13 -121G>A, A643T, P779P and c.3283T>G) of the IL-12R beta 2 gene, and the development of type 1 diabetes or atopic asthma as representative Th1- and Th2- dominant diseases, respectively. The association study of each polymorphism of the IL-12R beta 1 or IL-12R beta 2 gene and type 1 diabetes or asthma showed that these IL-12R genes did not contribute to the development of type 1 diabetes or asthma in the Japanese population. Further analysis in individuals with susceptibility to intracellular pathogens may elucidate the importance of the IL-12R genes.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ISSN:0093-7711
DOI:10.1007/s00251-003-0568-7