The role of B cells in immunity has been mainly related to the generation of antibodies and formation of immune complexes for a long period of time.
Indeed, in situ formation of immune complexes is a well-recognised mechanism of renal injury, as observed in systemic autoimmune disorders (Migliorini et al. 2002).
In vivo research utilising murine models susceptible to the development of metal-induced autoimmunity report that exposure to iHg results in a lupus-like syndrome, whilst mice exposed to MeHg develop autoimmunity without the formation of immune complexes.
The binding of anti-Gal, present in large amounts in humans, to the α-gal epitopes on the vaccinating virus or on the glycoprotein vaccines results in formation of immune complexes.
Initially, the attraction of antibodies was their specificity for target antigens; however, it is now appreciated that the downstream consequences of engaging antigen, after the formation of immune complexes, is crucial to clinical outcomes in vivo.
Activation of Rho has been shown to regulate actin polarization and the formation of immune synapses in DC [48].
The disease is characterized by autoantibody production against self, formation of immune complexes, and subsequent tissue inflammation in multiple organs such as the skin, joints, kidneys and heart.
Under these two circumstances, the formation of immune complex deposits in the glomerular capillary basement membrane may cause serious kidney damage.
The second mechanism is an opsonization process, involving the formation of immune complexes with ADAMTS13, which are subsequently cleared by phagocytes [2], [3].
Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease characterized by production of pathogenic anti-nuclear antibodies (ANA), resulting in the formation of immune complexes.
During persistent chronic viral infections, simultaneous antibody and virus production occurs, creating the conditions for the formation of immune complexes and the subsequent erythrocyte adherence.
