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Gene Review:

Aod1 - autoimmune ovarian dysgenesis 1

Mus musculus

Roper, R.J. et al., Wardell, B.B. et al., Roper, R.J. et al., Teuscher, C. et al., Scalzo, C.M. et al.

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Disease relevance of Aod1

Congenic mapping studies revealed that Aod1 controls susceptibility to oophoritis and comprises two linked QTL with opposing allelic effects [1].
Mice thymectomized at three days of age (D3Tx) develop during adulthood a variety of organ-specific autoimmune diseases, including autoimmune ovarian dysgenesis (AOD) [2].

High impact information on Aod1

In genetically susceptible strains of mice, such as A/J and (C57BL/6J x A/J)F1 hybrids, neonatal thymectomy-induced autoimmune ovarian dysgenesis (AOD) is characterized by the development of antiovarian autoantibodies, oophoritis, and atrophy [3].
Aod1, the immunoregulatory locus controlling abrogation of tolerance in neonatal thymectomy-induced autoimmune ovarian dysgenesis, maps to mouse chromosome 16 [2].
The D3Tx model of AOD is unique in that disease induction depends exclusively on perturbation of the normal developing immune system, is T-cell-mediated, and is strain specific [2].
Aod1 controlling day 3 thymectomy-induced autoimmune ovarian dysgenesis in mice encompasses two linked quantitative trait loci with opposing allelic effects on disease susceptibility [1].
Quantitative trait loci (QTL) linkage analysis using a B6AF(1) x C57BL/6J backcross population verified Aod1 and Aod2 that were previously mapped as qualitative traits [4].

Anatomical context of Aod1

Day 3 thymectomy (D3Tx) results in a loss of peripheral tolerance mediated by CD4(+)CD25(+) T cells and the development of autoimmune ovarian dysgenesis (AOD) in A/J and (C57BL/6J x A/J)F(1) (B6AF(1)) hybrids but not in C57BL/6J mice [4].

Associations of Aod1 with chemical compounds

Source of high testosterone levels associated with autoimmune ovarian dysgenesis in neonatally thymectomized B6A mice [5].

Other interactions of Aod1

Additionally, three new QTL intervals, Aod3, Aod4, and Aod5, on chromosomes 1, 2, and 7, respectively, influencing specific subphenotypes of AOD were identified [4].

Analytical, diagnostic and therapeutic context of Aod1

Interacting quantitative trait loci control loss of peripheral tolerance and susceptibility to autoimmune ovarian dysgenesis after day 3 thymectomy in mice [4].

References

Aod1 controlling day 3 thymectomy-induced autoimmune ovarian dysgenesis in mice encompasses two linked quantitative trait loci with opposing allelic effects on disease susceptibility. Roper, R.J., McAllister, R.D., Biggins, J.E., Michael, S.D., Min, S.H., Tung, K.S., Call, S.B., Gao, J., Teuscher, C. J. Immunol. (2003) [Pubmed]
Aod1, the immunoregulatory locus controlling abrogation of tolerance in neonatal thymectomy-induced autoimmune ovarian dysgenesis, maps to mouse chromosome 16. Wardell, B.B., Michael, S.D., Tung, K.S., Todd, J.A., Blankenhorn, E.P., McEntee, K., Sudweeks, J.D., Hansen, W.K., Meeker, N.D., Griffith, J.S. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
Aod2, the locus controlling development of atrophy in neonatal thymectomy-induced autoimmune ovarian dysgenesis, co-localizes with Il2, Fgfb, and Idd3. Teuscher, C., Wardell, B.B., Lunceford, J.K., Michael, S.D., Tung, K.S. J. Exp. Med. (1996) [Pubmed]
Interacting quantitative trait loci control loss of peripheral tolerance and susceptibility to autoimmune ovarian dysgenesis after day 3 thymectomy in mice. Roper, R.J., Ma, R.Z., Biggins, J.E., Butterfield, R.J., Michael, S.D., Tung, K.S., Doerge, R.W., Teuscher, C. J. Immunol. (2002) [Pubmed]
Source of high testosterone levels associated with autoimmune ovarian dysgenesis in neonatally thymectomized B6A mice. Scalzo, C.M., Michael, S.D. Biol. Reprod. (1988) [Pubmed]

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