Final answer:
The replacement of a self-reactive antigen receptor with a non-self-reactive one in B cells is called receptor editing. This process prevents autoimmunity by allowing B cells to revise their receptors rather than being destroyed. It's part of the negative selection to ensure self-tolerance in the immune response.
Step-by-step explanation:
The process of replacing a self-reactive antigen receptor with a non-self-reactive receptor in developing B cells is referred to as receptor editing. This mechanism is crucial for ensuring that B cells do not attack the body's own tissues, thereby preventing autoimmunity. Receptor editing is a part of the negative selection phase during B cell maturation. During this process, if a B cell receptor (BCR) is found to be self-reactive, the B cell gets a chance to edit its receptors instead of being immediately destroyed. This happens in the bone marrow and involves additional gene rearrangements that can lead to the production of a new, non-reactive BCR.
Two alternate mechanisms that are also part of B cell tolerance include clonal deletion, which eliminates self-reactive B cells via apoptosis, and clonal anergy, which renders the B cell nonfunctional without killing it. These mechanisms are essential for preventing B cells from attacking the body's own cells and for maintaining immune system balance.
The diversity of B cell receptors is achieved through gene rearrangement, specifically the recombination of V, D, and J gene segments at the DNA level, allowing for a multitude of unique antigen-specific receptors to be produced.