The general consensus is that autoimmune diseases have a multifactorial aetiology, depending on both genetic and environmental factors. Microbial agents or viruses can induce autoimmune diseases by a variety of mechanisms.¹ For example, proteins of certain infectious agents can act as polyclonal activators on unique lymphocyte subsets. Viruses can preferentially infect/destroy a particular T cell subset, leading to an imbalance in the immune response. Several microbial agents have been found to encode superantigens that can selectively activate subset(s) of T cells. Microbes can also direct the release of cytokines and chemokines, which can act as growth, differentiation, or chemotactic factors for different cell populations and regulate expression of major histocompatibility complex class I and class II as well as costimulatory molecules.²

The healthy immune system is tolerant of the molecules of which the body is composed. However, one can find that among the major antigens recognised during a wide variety of bacterial, viral, and parasitic diseases, many belong to conserved protein families, sharing extensive sequence identity or conformational fits, with the host’s molecules—namely, molecular mimicry. Antigenic similarity of the linear amino acid sequences of either molecule or their conformational structure between antigens of infectious agents and host tissues might trigger an immune response against the shared determinant. As a result, the tolerance to autoantigens breaks down, and the pathogen-specific immune response that is generated, cross reacts with host structures to cause tissue damage and disease. A role for molecular mimicry in the pathogenesis of autoimmune diseases has recently been shown in several animal models such as allergic encephalomyelitis, experimental myocarditis, and experimental autoimmune uveitis and keratitis.²

The classical antiphospholipid syndrome (APS) is characterised by the presence of antiphospholipid antibodies (aPL) which bind target phospholipid molecules, mainly through β_{2 …}