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No Evidence for Linkage in Swedish Multiplex T1DM Families to IL12B on Chromosome 5q33‐34
Author(s) -
HOLM PERNILLA,
LUTHMAN HOLGER,
KOCKUM INGRID
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1288.057
Subject(s) - nod mice , interleukin 12 , type 1 diabetes , immunology , autoimmune disease , chromosome 12 , medicine , gene , genetics , chromosome , biology , diabetes mellitus , endocrinology , cytotoxic t cell , in vitro , antibody
A bstract : Type 1 diabetes mellitus (T1DM) is an autoimmune disease in which the β cells in the pancreas are destroyed by the body's own immune system. IL12 plays a role in pathological situations, such as septic shock, tissue damage during inflammation, and organ‐specific autoimmune diseases. In NOD mice, administration of IL12 induces T1DM and administration of IL12 antagonists prevents T1DM. Linkage and association of IL12 to T1DM have been reported previously. We are unable to replicate this linkage on chromosome 5q33‐34 in 184 Swedish families. Further, we exclude a gene with λ s > 1.4 from this region. Together with previously published findings, these data make IL12 an unlikely major susceptibility gene for T1DM.