Developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin alters postnatal T cell phenotypes and T cell function and exacerbates autoimmune lupus in 24-week-old SNF1 mice.
Developmental exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin alters postnatal T cell phenotypes and T cell function and exacerbates autoimmune lupus in 24-week-old SNF1 mice.
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DOI:
10.1002/bdra.20603
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发表时间:
2009-10
影响因子:
--
通讯作者:
Gogal, Robert M., Jr.
中科院分区:
文献类型:
--
作者:
Mustafa, Amjad;Holladay, Steven D.;Goff, Matthew;Witonsky, Sharon;Kerr, Richard;Weinstein, Danielle A.;Karpuzoglu-Belgin, Ebru;Gogal, Robert M., Jr.
Untreated, more than 95% of female SWR × NZB: F1 (SNF1) mice spontaneously develop a fatal lupus-like glomerulonephritis by 8 months-of-age, while disease onset in males is much slower. Timed-pregnant SNF1 mice (10/treatment) were exposed to TCDD on gestational day (GD) 12 by oral maternal gavage with 0, 40 or 80 μg/kg TCDD. Offspring of the TCDD-exposed dams showed numerous alterations in T lineage cells at 24 weeks-of-age. Females but not males showed decreased CD4+8+ and increased CD4−8− thymocytes. Females also showed increased autoreactive CD4+Vβ17a+ axillary and inguinal lymph node T cells. Con-A stimulated splenocytes from prenatal TCDD-treated mice produced decreased IL-17 in the females while males showed increased IL-2 and IFN-γ, and diminished IL-4. Mitogen-stimulated pan-lymphoproliferative responses were significantly increased across sex by TCDD. Anti-IgG and anti-C3 immune complex deposition in kidneys was present in the males after TCDD, and visibly worsened in females. Developmental TCDD exposure can permanently alter T lymphopoiesis in autoimmune-prone SNF1 mice. The alteration profile is beyond the classic immune suppression response, to also include exacerbation and induction of a lupus-like autoimmune disease.
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影响因子:
4.4
作者:
Kang, Hee-Kap;Liu, Michael;Datta, Syamal K.
通讯作者:
Datta, Syamal K.
DOI:
10.1016/s0192-0561(99)00053-3
发表时间:
1999-12-01
期刊:
INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY
影响因子:
--
作者:
Hundeiker, C;Pineau, T;Esser, C
通讯作者:
Esser, C
DOI:
10.4049/jimmunol.181.4.2382
发表时间:
2008-08-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
Marshall NB;Vorachek WR;Steppan LB;Mourich DV;Kerkvliet NI
通讯作者:
Kerkvliet NI
影响因子:
4.4
作者:
Bagavant, H;Thompson, C;Tung, KSK
通讯作者:
Tung, KSK
影响因子:
13
作者:
Billiau, Alfons
通讯作者:
Billiau, Alfons