To aid one’s understanding of this article, I would like to briefly
introduce the method that researchers used to determine whether C3 synthesized
within the synovium in joints is important in promoting inflammation,
specifically for antibody-mediated arthritis in a mouse model.
First, they made four bone marrow chimeras between normal
and non-C3 mice. Wild type bone marrow was injected into non-C3 mouse (C3 only
in bone marrow); non-C3 bone marrow was injected into non-C3 mouse (control);
non-C3 bone marrow was injected into wild type mouse (C3 only in circulation); .
Wild type bone marrow was injected into wild type mouse (control). *Refer to Figure 1 (A) for visual aid.
Because antibodies can be shared between animals, serum that
contains antibody from sever arthritic mouse was introduced into those chimeras’
ankle joint to elicit arthritic reaction. Immunofluorescence staining against
C3 was used to detect C3 deposition in the joint (collagen). Enzyme-linked
immunosorbent assay (ELISA) was used to measure the amount of circulating C3.
They also made parabiotic mice (Parabiosis is a surgical union of two organisms allowing
sharing of the
blood circulation.) to see whether C3 had to be produced locally within the
joint, or whether it could be made at distant sites and transported to the
joint via the circulation. Non-C3 and WT mice (no C3 in bone marrow) were
sutured together to share the circulation. WT mouse was radiated to induce C3
production via parenchymal cells. The goal here was to introduce C3 to non-C3
mouse via circulation from distant site and compare those two mice’s reaction elicited
by antibodies from arthritic mouse. *Refer
to Figure 3 and 4 for visual aid.
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