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Passive transfer of collagen arthritis can be performed with a critical mixture of a number of anti-collagen type II monocloclonal antibodies, including complement binding IgG2a [ 26, 27].
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This could be attributed to hydroxyapatite crystallites in collagen fibrils which restricted the deformation of the collagen fibril network, and the load transfer of the collagen to the higher modulus mineral component of the composite.
Adoptive transfer of a collagen-specific T-cell hybridoma transduced to express anti-TNF single chain antibodies or IL-12 p40, or splenocytes from arthritic animals expressing TNF receptor or TGF-α all cause significant immune changes and ameliorate the disease [ 18- 22].
In tissues that are rich in macromolecules (which is typically the case in fibrosis due to the presence of collagen), the transfer of magnetization expressed as the "magnetization transfer ratio" or MTR will be high.
In addition, arthritis was induced in BALB/c and DBA/1 mice by passive transfer of anti-type II collagen mAb and immunisation with type II collagen, respectively.
Adoptive transfer of antibodies to citrullinated collagen frequently induced arthritis in naïve mice, however, only when co-administered with antibodies to unmodified collagen [ 118].
Since the films will be rolled into tubes with concentric layers of collagen, nutrient transfer through the collagen films is quite crucial.
For the collagen IV cultures, iPSC derived EBs were triturated and transferred to collagen IV-coated flasks [BD Biosciences].
Following transfer of anti-type II collagen monoclonal antibodies into factor B-deficient mice, only modest inflammation results as compared with wild-type mice.
The aim of the present study was to investigate the therapeutic effects of ALP in an arthritis model induced by the transfer of monoclonal antibodies (mAbs) to collagen type II (CII).
After each physical trituration, the muscles were transferred in a new well, to get rid of collagen wisps and hyper-contracted fibers.
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