Final answer:
MHC class I and II molecules gain their diversity from genetic polymorphisms, particularly in the regions that form the antigen-binding cleft. This variability allows the immune system to recognize a broad array of antigens. The diversity is encoded in the genome and further increased by mechanisms such as gene conversion and recombination.
Step-by-step explanation:
MHC class I and MHC class II molecules derive their diversity from the variability in their antigen-binding cleft, which is crucial for presenting different antigens to the immune system. MHC I molecules have an antigen-binding cleft formed by the α1 and α2 domains and are found on all nucleated cells. They present both normal self-antigens and abnormal or nonself pathogens to effector T cells involved in cellular immunity. On the other hand, MHC II molecules, which are only found on professional antigen-presenting cells like macrophages, dendritic cells, and B cells, have an antigen-binding cleft formed by the α1 and β1 domains. They present abnormal or nonself pathogen antigens for the initial activation of T cells.
Both MHC I and MHC II molecules are transmembrane glycoproteins that exhibit polymorphism, especially in the regions that form the antigen-binding cleft. This polymorphism is a result of multiple alleles within the MHC gene family, which leads to the expression of a diverse set of molecules, each capable of binding to a distinct set of peptides. This genetic diversity is further increased by the process of gene conversion and recombination, which contributes significantly to the variability in the populations. It is this genetic variation that equips the immune system with the ability to recognize a wide spectrum of pathogens.