Editing Rheumatoid arthritis (section)

===Amplification in the synovium===
Once the generalized abnormal immune response has become established – which may take several years before any symptoms occur – plasma cells derived from B lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in large quantities. These activate macrophages through Fc receptor and complement binding, which is part of the intense inflammation in RA.<ref>{{cite book|editor-last1=Makowski |editor-first1=Gregory|vauthors=Boldt AB, Goeldner I, de Messias-Reason IJ |pmid=22397030|chapter=Relevance of the lectin pathway of complement in rheumatic diseases|doi=10.1016/B978-0-12-394317-0.00012-1|volume=56 |pages=105–153|year=2012| title = Advances in Clinical Chemistry|publisher=Elsevier |isbn=978-0-12-394317-0 }}{{subscription required}}</ref> Binding of an autoreactive antibody to the Fc receptors is mediated through the antibody's N-glycans, which are altered to promote inflammation in people with RA.<ref name = "immune_glycan"/>{{rp|8}}

This contributes to local inflammation in a joint, specifically the synovium with [[edema]], [[vasodilation]] and entry of activated T-cells, mainly CD4 in microscopically nodular aggregates and CD8 in microscopically diffuse infiltrates.<ref name=":02">{{cite journal | vauthors = Jonsson AH, Zhang F, Dunlap G, Gomez-Rivas E, Watts GF, Faust HJ, Rupani KV, Mears JR, Meednu N, Wang R, Keras G, Coblyn JS, Massarotti EM, Todd DJ, Anolik JH, McDavid A, Wei K, Rao DA, Raychaudhuri S, Brenner MB | title = Granzyme K<sup>+</sup> CD8 T cells form a core population in inflamed human tissue | journal = Science Translational Medicine | volume = 14 | issue = 649 | pages = eabo0686 | date = June 2022 | pmid = 35704599 | pmc = 9972878 | doi = 10.1126/scitranslmed.abo0686 }}</ref>

Synovial macrophages and [[dendritic cell]]s function as [[antigen-presenting cell]]s by expressing MHC class II molecules, which establishes the immune reaction in the tissue.<ref name=":02" />