Interleukin-4 deficiency does not exacerbate disease in NOD mice.
To investigate the role of interleukin (IL)-4 in the regulation of autoimmune diabetes, we crossed the IL-4 knock-out mutation onto the NOD genetic background. This experiment was accelerated by typing for microsatellites linked to known diabetes susceptibility (Idd) loci, and included a control backcross of the wild-type 129/SvJ-derived IL-4 gene, the original target locus. We also crossed the mutation into the BDC2.5 transgenic line, a diabetes model that carries the rearranged T-cell receptor genes from a diabetogenic T-cell clone. The IL-4-null mutation did not accelerate or intensify insulitis in regular NOD mice or in the BDC2.5 transgenic model; it also had no effect on the timing or frequency of the transition to overt diabetes. These data indicate that IL-4 plays no required role in controlling the aggressiveness of murine diabetes.
Wang
B
B
Institut de Génétique et de Biologie Moléculaire et Cellulaire, C.U. de Strasbourg, France.
Gonzalez
A
A
Höglund
P
P
Katz
J D
JD
Benoist
C
C
Mathis
D
D
D000483:Alleles; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology*; D006824:Hybridization, Genetic; D015994:Incidence; D007249:Inflammation / Q000473:pathology; D015847:Interleukin-4 / Q000172:deficiency* / Q000235:genetics; D015848:Interleukin-5 / Q000096:biosynthesis; D007515:Islets of Langerhans / Q000473:pathology; D051379:Mice; D016688:Mice, Inbred NOD / Q000502:physiology*; D018345:Mice, Knockout / Q000235:genetics; D018895:Microsatellite Repeats
D015848:Interleukin-5; D015847:Interleukin-4