Ans. is 'b' i.e., Autoimmune disorders* Molecular mimicry is defined as the structural similarity between foreign antigens and self-antigens, because of which T cells and B cells directed against foreign antigens cross react with self antigens resulting in autoimmunity.* Molecular mimicry does not always demand a structural similarity between foreign antigens and self antigens. Sometimes electrostatic attraction between foreign antigen and MHC molecule can cause self antigen damage by immune response generated against foreign antigens.* Molecular mimicry is also possible between two recognized peptides that have similar antigenic surfaces in the absence of primary sequence homology. For example, specific single amino acid residues such as cysteine (creates di-sulfide bonds), arginine or lysine (form multiple hydrogen bonds), could be essential for T cell cross-reactivity.* Immunological tolerance is the ability to discriminate self-antigens from foreign antigens and to not produce antibodies against self-antigens* Loss of this immunological tolerance is generally considered as a initiation factor for autoimmunity* Immunological tolerance is generally established in foetus, soon after the pre-T cells leave the bone marrow and they reach the thymus* In thymus, any clone of T cell which binds only weekly to self-antigen i.e., MHC class I antigen is positively selected and is allowed to undergo maturation.* Any clone which binds avidly to one's own MHC class I molecules are negatively selected and apoptosis is induced. This is called as clonal deletion* For exposure to more antigens, this process is found to continue even in peripheral circulation. The clonal deletion analogue which happens in peripheral circulation is called as clonal anergy* B cell tolerance is mediated by VDJ rearrangements and somatic hypermutation* Failure of these immunological tolerance rules can result in autoimmunity