TY - JOUR
T1 - Abnormal Anterior Chamber Associated Immune Deviation (ACAID) in 129-strain mice
AU - Herndon, John
AU - Gibler, Therese S.
AU - Ferguson, Thomas A.
AU - Van Gelder, Russell N.
N1 - Funding Information:
Accepted 29 January 2005. Acknowledgment: This research was supported by a Research to Prevent Blindness Career Development Award (RVG), the Becker/AUPO/RPB Clinician-Scientist Award and NIH KO8 EY00403 (RVG) and NIH R01 EY06765 (TAF). Correspondence and reprint requests to: Russell N. Van Gelder, M.D., Ph.D., Department of Ophthalmology and Visual Sciences, Washington University Medical School, Campus Box 8096, 660 S. Euclid Ave., St. Louis, MO 63110. Tel: (314) 747 4251; Fax: (314) 747 5537; e-mail: [email protected]
PY - 2006/2
Y1 - 2006/2
N2 - Purpose: 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) × 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. Conclusion: 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.
AB - Purpose: 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) × 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. Conclusion: 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.
KW - ACAID
KW - Delayed hypersensitivity
KW - Ocular immune privilege
KW - Strain difference
KW - Tolerance
UR - http://www.scopus.com/inward/record.url?scp=33644761811&partnerID=8YFLogxK
U2 - 10.1080/09273940600556995
DO - 10.1080/09273940600556995
M3 - Article
C2 - 16507485
AN - SCOPUS:33644761811
SN - 0927-3948
VL - 14
SP - 7
EP - 12
JO - Ocular Immunology and Inflammation
JF - Ocular Immunology and Inflammation
IS - 1
ER -