An overview of the potential mechanism for the exposure of cryptic antigenic determinants leading to development of Abs to self-Ags in CR following solid organ Tx. Various risk factors such as surgical stress, viral and bacterial infections, mismatched HLA following solid organ transplantation induces tissue remodeling and exposure of cryptic self-antigenic determinants. This leads to cellular and humoral responses and upregulated expression of fibrotic signaling molecules and growth factors such as HIF1α, VEGF, FGF, etc. All these culminate to fibrosis and loss of function manifesting as CR of the allograft.