Microparticles That Form Immune Complexes as Modulatory Structures in Autoimmune Responses

Figure 3

Role of MPs in SLE. MPs can interact with B cells (LB) (a) during ontogeny-induced apoptosis (clonal deletion), secondary rearrangement, or BCR edition in cells whose BCRs recognize DNA with high affinity. (b) At the lymphoid organ level, MPs can also bind to an autoreactive BCR and induce anergy of LB or alternatively be endocytosed by these cells and induce a second signal through TLR9 and TLR7 by the DNA and RNA present on these structures. These recognition activate and differentiate B cells into plasma cells able to produce autoantibodies. (c) MPs can be internalized by plasmacytoid dendritic cells (pDCs) and through the recognition of nucleic acids produce type I IFNs and other cytokines such as IL-6. (d) MPs might compete with ACs to bind PS receptors on monocytes and macrophages (Mo/MΦ), which seem to contribute to the lower uptake of ACs observed in these patients. In addition, MPs can be a major source of autoantigens in SLE with the consequent generation of ICs; all this could eventually (1) produce and maintain the inflammatory immune response and (2) promote the damage of different tissues and organs in patients with SLE due to the exacerbated inflammatory process.

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