YOSHIKAWA Kunihiko Osaka University, Graduate School of Medicine, Professor, 医学系研究科, 教授 (20110851)
ITAMI Satoshi Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (30136791)
|Budget Amount *help
¥3,300,000 (Direct Cost : ¥3,300,000)
Fiscal Year 2001 : ¥1,300,000 (Direct Cost : ¥1,300,000)
Fiscal Year 2000 : ¥2,000,000 (Direct Cost : ¥2,000,000)
This is to study the role of T cells on IgE production in the model mouse for atopic dermatitis, using NC/nga, OVA, and anti-OVA TCR transgenic mice. As anti-OVA CD4 TCR transgenic mouse, OT-II (I-Ab restricted, C57BL/6) and as anti-OVA CDS TCR transgenic mouse, OT-I (H-2Kb restricted, C57BL/6) were introduced. Finally we established OT-II (H-2/nc, NC), OT-II(H-2bxnc, NC), OT-II(H-2b, C57BL/6), OT-I(H-2nc, NC) OT-I(H-2bxnc, NC), and OT-I(H-2b, C57BL/6).
Positive selection of transgenic OT-I- and OT-II-TCRs in the thymus of both H-2b(NC) and H-2b(C57bl/6) is normal. In addition there is hardly any difference between NC background and C57W/6 background in positive and partial negative selection observed in H-2bxnc.
T cells prepared from either NC and C57bl/6 background responded equally well to OVA in vitro. On the other hand, anti-OVA IgE production induced in vivo is very high in NC background of nonetransgenic mice. When mice are carrying transgenic anti-OVA TCR, it is of surprise that anti-OVA IgE production of C57BL/6 background is higher than that of NC background. Moreover, OT-I(H-2bxnc, NC) sometimes have dermatitis under our SPF condition.
From these findings, although NC background mice are high IgE producer, they do not produce IgE well at some combination of TCR. It might explain the reason why Some atopic dermatitis patient produce many kinds of specific IgE but others produce certain kinds of specific IgE.