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Genetic and nongenetic control of the immune response of mice to a synthetic glycolipid, stearylisomaltotetraose
Authors:E Lai  E A Kabat  L Mobraaten
Affiliation:1. Departments of Pharmacology, Microbiology, Human Genetics and Development, Neurology, and the Cancer Center/Institute for Cancer Research, Columbia University College of Physicians and Surgeons, New York, New York 10032 U.S.A.;2. The Jackson Laboratory, Bar Harbor, Maine 04609 U.S.A.;1. Department of Pharmacology, School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China;2. Department of Experimental Teaching Center, School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China;3. The First Affiliated Hospital of Anhui Medical University, Hefei, China;4. Anhui Public Health Clinical Center, Hefei, China;5. Department of Anatomy, School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei 230012, China;6. Institute of Prevention and Treatment of Rheumatoid Arthritis, Anhui University of Chinese Medicine, Hefei, Anhui, China;7. School of Chinese Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region
Abstract:Evidence for genetic control of antibody response to stearylisomaltotetraose (ST-IM4), a chemically defined synthetic glycolipid, was studied in various mouse strains. Anti-glycolipid antibodies were induced by repeated injections of ST-IM4 in complete Freund's adjuvant. C57BL and CBA/J mice were found to be good responders, while A/J, SJL/J, and AKR/J mice were poor responders. Responsiveness is independent of the H-2 genotype since AKR/J and CBA/J mice share the same H-2 locus. In addition, B10.A and B10.PL mice developed antibody levels similar to those of C57BL. The immunoglobulin heavy-chain locus (IgCH) was also found not to control antibody levels to ST-IM4 since C57BL and SJL/J mice share the same IgCH allotype. In C58/J mice, wide variation in response was observed among individual mice. Study of the response to ST-IM4 in 12 breeder pairs from different family lines of the C58/J colony also indicated that the regulation of the immune response to ST-IM4 is apparently more complex than can be explained by single gene control. C58 mice, unlike many other strains, had very low preimmune titers.
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