## Abstract Prepubertal castration of female NZB/NZW (B/W) hybrid mice did not influence mortality, whereas prepubertal castration of male B/W mice caused premature death and enhanced autoantibody formation. Prepubertal castration combined with the administration of sustained estradiol‐17‐β (E‐2) e
Clearance of sensitized erythrocytes in NZB/NZW mice Effects of castration and sex hormone treatment
✍ Scribed by Hannah Lustig Shear; Jirayr R. Roubinian; Paul Gil; Norman Talal
- Publisher
- John Wiley and Sons
- Year
- 1981
- Tongue
- English
- Weight
- 515 KB
- Volume
- 11
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The clearance of particulate immune complexes consisting of erythrocytes sensitized with IgG or complement was investigated in (NZB × NZW)F~1~ (B/W) mice. Treatment of castrated B/W mice with androgen or estrogen was able to modulate this clearance.
Young (3‐month‐old) male and female B/W mice cleared IgG‐sensitized mouse erythrocytes rapidly, whereas older males (13 months) and females (7 months) showed a marked impairment in their ability to clear these cells. In addition, erythrocytes sensitized with complement in the absence of antibody were cleared within 5 min in young B/W mice. Older mice showed a greater and more rapid clearance rate of these cells.
Castrated female B/W mice treated with androgen implants from three weeks of age showed improved clearance of IgG‐sensitized erythrocytes at 7 months, whereas estrogen‐treated male mice showed delayed clearance.
These results suggest an age‐dependent defect in the clearance of IgG‐sensitized particles, perhaps due to diminished levels of serum complement and/or saturation of Fc receptors. In addition, there is an alteration in the clearance of complement‐sensitized erythrocytes which may be related to changes in macrophage activity or enzyme inactivators of C3 and C4. The possible mechanisms responsible for the hormonal modulation of clearance are discussed in relation to the known ability of these hormones to influence autoimmune diseases.
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