This chapter discusses the Type II collagen present in the articular cartilage of the hind paws and activates the complement system. This activation leads to the generation of complement components, C3a and C5a. C3a can increase vascular permeability and allow for the trafficking of sensitized lymphocytes into the joint space. These sensitized lymphocytes can proliferate in the joint space and secrete lymphokines that may induce the proliferation of synovial tissue. C5a can induce migration of inflammatory cells into the joint space. These inflammatory cells contain connective tissue-degrading enzymes (collagenase, elastase, and neutral and acid cathepsins) that can induce joint destruction. In this mechanism, anticollagen immunoglobulin G (IgG) plays a critical role in initiating the disease and cell-mediated immunity, which is required for sustaining the lesion. Evidence supporting this hypothesis is presented. For histologic analysis, the hind paws are fixed in buffered formalin and decalcified in formic acid. The tissue is embedded in paraffin or plastic, and the sections are stained with hematoxylin and eosin.
ASJC Scopus subject areas
- Molecular Biology