Abnormal anterior chamber associated immune deviation (ACAID) in 129-strain mice.
OBJECTIVE
To characterize anterior chamber immune deviation (ACAID) in 129-strain and mixed 129-strain mice.


METHODS
ACAID was assayed using standard protocols with herpes simplex-1 (HSV-1) and trinitrophenol-hapten-spleen cells (TNP-spleen) in C57B1/6, 129P2, 129X1, and intercrossed strains. Systemic tolerance induction was assayed using an ultraviolet light skin tolerance protocol to 2,-4,6-trinitro-l-chlorobenzene (TNCB).


RESULTS
129X1 and C57Bl/6xl29Xl Fl mice did not show ACAID to HSV-1. C57Bl/6xl29P2 mice did not show ACAID to TNP-spleen. C57Bl/6xl29P2 mice did show normal peripheral immune deviation to TNCB. (C57Bl/6xl29Xl) x C57B1/6 N2 backcrossed mice showed a bimodal ACAID response to HSV-1 suggesting a single dominant allele in the 129X1 background responsible for suppressing ACAID.


CONCLUSIONS
ACAID to multiple antigens is significantly reduced in 129-strain mice and their outcrossed progeny. Since 129-strain embryonic stem cells are widely used to generate knockout and transgenic mice, care must be taken to extensively backcross resultant strains in order to assess the effect of particular genes on ACAID.
Herndon
John
J
Department of Ophthalmology and Visual Sciences, Washington University Medical School, Saint Louis, MO 63110, USA.
Gibler
Therese S
TS
Ferguson
Thomas A
TA
Van Gelder
Russell N
RN
D000818:Animals; D000867:Anterior Chamber / Q000276:immunology*; D017951:Antigen Presentation / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D004195:Disease Models, Animal; D018259:Herpesvirus 1, Human / Q000276:immunology; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007108:Immune Tolerance; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology