Emergence of antiplatelet autoantibodies.

Platelet proteins are cleaved to peptides by an antigen-presenting cell (APC) and expressed on the APC cell surface via MHC class II molecules. The T-cell receptor (TCR) of the Th cell can then bind the peptide-MHC complex and signal activation that upregulates CD154 (CD40 ligand) to interact with CD40 on the APC and cause additional costimulatory interactions to occur. The activated Th cell produces cytokines (interleukin-2 and interferon-γ) that promote B-cell differentiation and antibody production.