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Immunization with cationized BSA inhibits progression of disease in ApoBec-1/LDL receptor deficient mice with manifest atherosclerosis.

Kolbus, Daniel LU ; Wigren, Maria LU ; Ljungcrantz, Irena LU ; Söderberg, Ingrid LU ; Alm, Ragnar LU ; Björkbacka, Harry LU ; Nilsson, Jan LU and Nordin Fredrikson, Gunilla LU (2011) In Immunobiology 216. p.663-669
Abstract
Immune responses against modified self-antigens generated by hypercholesterolemia play an important role in atherosclerosis identifying the immune system as a possible novel target for prevention and treatment of cardiovascular disease. It has recently been shown that these immune responses can be modulated by subcutaneous injection of adjuvant. In the present study we immunized 25-week old ApoBec-1/LDL receptor deficient mice with manifest atherosclerosis with adjuvant and two different concentrations of the carrier molecule cationized BSA (cBSA). Plasma levels of Th2-induced apolipoprotein B (apoB)/IgG1 immune complexes were increased in the cBSA immunized groups verifying induction of immunity against a self-antigen. Mice were... (More)
Immune responses against modified self-antigens generated by hypercholesterolemia play an important role in atherosclerosis identifying the immune system as a possible novel target for prevention and treatment of cardiovascular disease. It has recently been shown that these immune responses can be modulated by subcutaneous injection of adjuvant. In the present study we immunized 25-week old ApoBec-1/LDL receptor deficient mice with manifest atherosclerosis with adjuvant and two different concentrations of the carrier molecule cationized BSA (cBSA). Plasma levels of Th2-induced apolipoprotein B (apoB)/IgG1 immune complexes were increased in the cBSA immunized groups verifying induction of immunity against a self-antigen. Mice were sacrificed at 36 weeks of age and atherosclerosis was monitored by en face Oil red O staining of the aorta. Immunization with 100μg cBSA inhibited plaque progression, whereas the lower dose (50μg) did not. In addition, the higher dose induced a more stable plaque phenotype, indicated by a higher content of collagen and less macrophages and T cells in the plaques. Moreover, there was an increased ratio of Foxp3(+)/Foxp3(-) T cells in the circulation suggesting activation of a regulatory T cell response. In conclusion, we show that immunization with cBSA induces an immune response against apoB as well as an activation of Treg cells. This was associated with development of a more stable plaque phenotype and reduced atherosclerosis progression. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Immunobiology
volume
216
pages
663 - 669
publisher
Elsevier
external identifiers
  • wos:000296936800002
  • pmid:21247654
  • scopus:79955528094
ISSN
1878-3279
DOI
10.1016/j.imbio.2010.11.003
language
English
LU publication?
yes
id
ffce8da9-ca1d-4ffc-a2e5-fc82ddad80d1 (old id 1777298)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21247654?dopt=Abstract
date added to LUP
2011-02-01 15:07:17
date last changed
2017-01-01 05:24:45
@article{ffce8da9-ca1d-4ffc-a2e5-fc82ddad80d1,
  abstract     = {Immune responses against modified self-antigens generated by hypercholesterolemia play an important role in atherosclerosis identifying the immune system as a possible novel target for prevention and treatment of cardiovascular disease. It has recently been shown that these immune responses can be modulated by subcutaneous injection of adjuvant. In the present study we immunized 25-week old ApoBec-1/LDL receptor deficient mice with manifest atherosclerosis with adjuvant and two different concentrations of the carrier molecule cationized BSA (cBSA). Plasma levels of Th2-induced apolipoprotein B (apoB)/IgG1 immune complexes were increased in the cBSA immunized groups verifying induction of immunity against a self-antigen. Mice were sacrificed at 36 weeks of age and atherosclerosis was monitored by en face Oil red O staining of the aorta. Immunization with 100μg cBSA inhibited plaque progression, whereas the lower dose (50μg) did not. In addition, the higher dose induced a more stable plaque phenotype, indicated by a higher content of collagen and less macrophages and T cells in the plaques. Moreover, there was an increased ratio of Foxp3(+)/Foxp3(-) T cells in the circulation suggesting activation of a regulatory T cell response. In conclusion, we show that immunization with cBSA induces an immune response against apoB as well as an activation of Treg cells. This was associated with development of a more stable plaque phenotype and reduced atherosclerosis progression.},
  author       = {Kolbus, Daniel and Wigren, Maria and Ljungcrantz, Irena and Söderberg, Ingrid and Alm, Ragnar and Björkbacka, Harry and Nilsson, Jan and Nordin Fredrikson, Gunilla},
  issn         = {1878-3279},
  language     = {eng},
  pages        = {663--669},
  publisher    = {Elsevier},
  series       = {Immunobiology},
  title        = {Immunization with cationized BSA inhibits progression of disease in ApoBec-1/LDL receptor deficient mice with manifest atherosclerosis.},
  url          = {http://dx.doi.org/10.1016/j.imbio.2010.11.003},
  volume       = {216},
  year         = {2011},
}