Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice
Samo za registrovane korisnike
2011
Autori
Živković, IrenaStojanović, Marijana
Petrušić, Vladimir
Inić-Kanada, Aleksandra
Dimitrijević, Ljiljana
Članak u časopisu (Objavljena verzija)
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
Problem The antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by vascular thrombosis and/or pregnancy complications (lower fecundity and lower litter size), as well as by an increase in anti-beta(2) glycoprotein I (beta(2)GPI)-specific autoantibody titer. We have investigated how the genetic background of the immune system [T helper (Th) prevalence] and the type of animal model of APS influence the induced pathology. Method of Study Antiphospholipid syndrome induced by tetanus toxoid (TTd) hyper-immunization and by intravenous application of monoclonal anti-beta(2)GPI-specific antibody 26 was compared in C57BL/6 (Th1 prone) and BALB/c (Th2 prone) mice. Results Tetanus toxoid hyper-immunization of BALB/c mice led to reduction in fertility, but in C57BL/6 mice a decrease in fecundity occurred. In both cases, pathology was caused by anti-beta(2)GPI antibodies, the production of which was adjuvant and strain dependent. Conclusion We conclude that TTd immunizati...on and i.v. application of monoclonal antibody 26 induced the same reproductive pathology and that the type of pathology is strain dependent.
Ključne reči:
Antiphospholipid syndrome / fecundity / fertility / mouse strainIzvor:
American Journal of Reproductive Immunology, 2011, 65, 5, 492-502Izdavač:
- Wiley-Blackwell, Hoboken
Finansiranje / projekti:
- Alergeni, antitela, enzimi i mali fiziološki značajni molekuli: dizajn, struktura, funkcija i značaj (RS-172049)
- Ispitivanje strukture i funkcije biološki važnih makromolekula u fiziološkim i patološkim stanjima (RS-142020)
DOI: 10.1111/j.1600-0897.2010.00922.x
ISSN: 1046-7408
PubMed: 21029246
WoS: 000289172000005
Scopus: 2-s2.0-79953718040
Institucija/grupa
TorlakTY - JOUR AU - Živković, Irena AU - Stojanović, Marijana AU - Petrušić, Vladimir AU - Inić-Kanada, Aleksandra AU - Dimitrijević, Ljiljana PY - 2011 UR - http://intor.torlakinstitut.com/handle/123456789/321 AB - Problem The antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by vascular thrombosis and/or pregnancy complications (lower fecundity and lower litter size), as well as by an increase in anti-beta(2) glycoprotein I (beta(2)GPI)-specific autoantibody titer. We have investigated how the genetic background of the immune system [T helper (Th) prevalence] and the type of animal model of APS influence the induced pathology. Method of Study Antiphospholipid syndrome induced by tetanus toxoid (TTd) hyper-immunization and by intravenous application of monoclonal anti-beta(2)GPI-specific antibody 26 was compared in C57BL/6 (Th1 prone) and BALB/c (Th2 prone) mice. Results Tetanus toxoid hyper-immunization of BALB/c mice led to reduction in fertility, but in C57BL/6 mice a decrease in fecundity occurred. In both cases, pathology was caused by anti-beta(2)GPI antibodies, the production of which was adjuvant and strain dependent. Conclusion We conclude that TTd immunization and i.v. application of monoclonal antibody 26 induced the same reproductive pathology and that the type of pathology is strain dependent. PB - Wiley-Blackwell, Hoboken T2 - American Journal of Reproductive Immunology T1 - Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice EP - 502 IS - 5 SP - 492 VL - 65 DO - 10.1111/j.1600-0897.2010.00922.x ER -
@article{ author = "Živković, Irena and Stojanović, Marijana and Petrušić, Vladimir and Inić-Kanada, Aleksandra and Dimitrijević, Ljiljana", year = "2011", abstract = "Problem The antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by vascular thrombosis and/or pregnancy complications (lower fecundity and lower litter size), as well as by an increase in anti-beta(2) glycoprotein I (beta(2)GPI)-specific autoantibody titer. We have investigated how the genetic background of the immune system [T helper (Th) prevalence] and the type of animal model of APS influence the induced pathology. Method of Study Antiphospholipid syndrome induced by tetanus toxoid (TTd) hyper-immunization and by intravenous application of monoclonal anti-beta(2)GPI-specific antibody 26 was compared in C57BL/6 (Th1 prone) and BALB/c (Th2 prone) mice. Results Tetanus toxoid hyper-immunization of BALB/c mice led to reduction in fertility, but in C57BL/6 mice a decrease in fecundity occurred. In both cases, pathology was caused by anti-beta(2)GPI antibodies, the production of which was adjuvant and strain dependent. Conclusion We conclude that TTd immunization and i.v. application of monoclonal antibody 26 induced the same reproductive pathology and that the type of pathology is strain dependent.", publisher = "Wiley-Blackwell, Hoboken", journal = "American Journal of Reproductive Immunology", title = "Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice", pages = "502-492", number = "5", volume = "65", doi = "10.1111/j.1600-0897.2010.00922.x" }
Živković, I., Stojanović, M., Petrušić, V., Inić-Kanada, A.,& Dimitrijević, L.. (2011). Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice. in American Journal of Reproductive Immunology Wiley-Blackwell, Hoboken., 65(5), 492-502. https://doi.org/10.1111/j.1600-0897.2010.00922.x
Živković I, Stojanović M, Petrušić V, Inić-Kanada A, Dimitrijević L. Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice. in American Journal of Reproductive Immunology. 2011;65(5):492-502. doi:10.1111/j.1600-0897.2010.00922.x .
Živković, Irena, Stojanović, Marijana, Petrušić, Vladimir, Inić-Kanada, Aleksandra, Dimitrijević, Ljiljana, "Induction of APS after TTd Hyper-Immunization has a Different Outcome in BALB/c and C57BL/6 Mice" in American Journal of Reproductive Immunology, 65, no. 5 (2011):492-502, https://doi.org/10.1111/j.1600-0897.2010.00922.x . .