Результаты исследований: Научные публикации в периодических изданиях › статья
Oral administration of Domain-I of beta-2glycoprotein-I induces immunological tolerance in experimental murine antiphospholipid syndrome. / Shemer, A.; Shoenfeld, Y.; Blank, M.
в: Journal of Autoimmunity, Том 99, 2019, стр. 98-103.Результаты исследований: Научные публикации в периодических изданиях › статья
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TY - JOUR
T1 - Oral administration of Domain-I of beta-2glycoprotein-I induces immunological tolerance in experimental murine antiphospholipid syndrome.
AU - Shemer, A.
AU - Shoenfeld, Y.
AU - Blank, M.
PY - 2019
Y1 - 2019
N2 - It is well established that the humoral immunity in antiphospholipid syndrome (APS) is presented by circulating pathogenic anti-β2GPI autoantibodies targeting mainly domain I of the β2GPI protein, playing a major role in the disease pathogenesis. Previously, we have demonstrated that treatment of experimental APS mice with tolerogenic dendritic cells loaded with domain-I was more efficient in tolerance induction than with the whole molecule or domain-V. In the current study we had orally administered a domain-I derivative of the β2GPI molecule, as a new therapeutic approach to induce oral tolerance in this mouse model of APS. BALB/c mice immunized with β2GPI, were fed with either domain-I, domain-V derivative or the complete β2GPI protein. β2GPI immunized mice developed experimental APS which were fed with domain-I significantly had decreased fetal loss (p < 0.004), a lower size of thrombi (p < 0.001) and lower circulating anti-β2GPI Abs in comparison to mice fed with domain-V or PBS (p < 0.002). Likewise, Do
AB - It is well established that the humoral immunity in antiphospholipid syndrome (APS) is presented by circulating pathogenic anti-β2GPI autoantibodies targeting mainly domain I of the β2GPI protein, playing a major role in the disease pathogenesis. Previously, we have demonstrated that treatment of experimental APS mice with tolerogenic dendritic cells loaded with domain-I was more efficient in tolerance induction than with the whole molecule or domain-V. In the current study we had orally administered a domain-I derivative of the β2GPI molecule, as a new therapeutic approach to induce oral tolerance in this mouse model of APS. BALB/c mice immunized with β2GPI, were fed with either domain-I, domain-V derivative or the complete β2GPI protein. β2GPI immunized mice developed experimental APS which were fed with domain-I significantly had decreased fetal loss (p < 0.004), a lower size of thrombi (p < 0.001) and lower circulating anti-β2GPI Abs in comparison to mice fed with domain-V or PBS (p < 0.002). Likewise, Do
M3 - Article
VL - 99
SP - 98
EP - 103
JO - Journal of Autoimmunity
JF - Journal of Autoimmunity
SN - 0896-8411
ER -
ID: 78468331