Induction of IgG Rheumatoid Factor (RF) Production by Antibody–antibody (RF-like) Immune Complexes: the Role of T cells, Complement and Fcγ Receptors

“…As in other immunologically-mediated disorders, the immunogenetic antecedents, antigenic characteristics of organic dusts, or the duration of avian exposure, and the intensity of antibody production, among several characteristics, may contribute to the appearance of different RF classes (41,(50)(51)(52)(53). In this context, some clinical and experimental observations have suggested that IgM RF may arise as a consequence of IC formation (35,54,55), and the production of monospecific, somatically mutated IgG or IgA RFs may be associated with chronic antigenic stimulation, as occurs in some infectious lung diseases (18).…”

Section: Discussionmentioning

confidence: 99%

IgM, IgG, and IgA rheumatoid factors in pigeon hypersensitivity pneumonitis

Araiza¹,

León

Retana

et al. 2007

Clinical Laboratory Analysis

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The association of rheumatoid factor (RF) and lung disease in several immunologically mediated conditions has suggested that it may be physiopathologically relevant. Since previous reports in hypersensitivity pneumonitis (HP) have dealt mainly with the immunoglobulin M (IgM) RF measurement, we studied such antibody activity in other immunoglobulins, to determine the IgG and IgA RF levels in pigeon-HP, and in asymptomatic breeders (AB) and rheumatoid arthritis (RA) as controls. RFs were measured in 35 HP patients, 41 AB, 31 RA controls, and 55 healthy donors by enzyme-linked immunosorbent assay (ELISA) using human or rabbit immunoglobulin G (IgG), anti-IgM, F(ab')2 of IgG, and IgA F(ab')2 conjugates. An affinity chromatography, fragment crystallizable (Fc) preparations of IgG, pepsin digestion, and Western blots were used to confirm RF specificity. We also evaluated anti-avian antibodies (AA) and cross-reacting antibodies. The HP group revealed positive IgM (51.4%), IgG (31.4%), and immunoglobulin A (IgA) (34.2%) RF tests, and these antibody values exceeded the AB reference levels (P<0.02). HP and RA showed a similar frequency and distribution of RFs. Possible immunoassay interferences were excluded. As in other immunologically mediated diseases, IgG and IgA RFs may play a pathogenic role in HP, amplifying the inflammatory reaction, immune-complex formation, and complement activation. IgM-RF producing cells that have been implicated in the presentation of self and foreign antigens, and T-cell activation might induce the isotype switching of RFs.

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“…Complement proteins can be produced locally in the synovial tissue (64), and activation of the complement system can cause inflammation by cytokine release following ligation of Fcγ receptors on macrophages (65). Complement has, in addition, been shown to have a role in the induction of the humoral immune response against T cell–dependent antigens (66, 67).…”

Section: Discussionmentioning

confidence: 99%