Question appears to ask whether a person’s own antibodies could serve as immunogens to their own immune system so that’s what this answer addresses. An Immunogen – Wikipedia is any substance capable of eliciting an immune response, i.e., target of an immune response. Though immunogen and Antigen – Wikipedia are often interchangeably used terms, key difference between the two is the final outcome. While both antigen and immunogen can bind an immune receptor, typically immunogen is used for something known to trigger an immune response.

Essential building blocks of life, proteins are far and away the singular focus of the human immune system, especially of the adaptive immune system, which consists of T and B cells. Antibodies are protein molecules so of course, they could be targets of immune responses, except there are inbuilt processes that serve as safeguards to minimize, not eliminate, such likelihood. Why minimize but not eliminate the likelihood antibodies could themselves be immunogens?

T cells are the master architects of human adaptive immune responses. B cells typically need T cell help to make antibodies, even antibodies against other antibodies. T cell help for B cells is usually called cognate, meaning the T cell ‘sees’ a portion of the same antigen as the B cell.

Antibodies, just like other protein molecules can be internalized by antigen presenting cells such as dendritic cells, macrophages and monocytes, get digested and their peptides presented to T cells within MHC molecules. However, normally, T cells with receptors specific for most of the peptide pieces generated from digesting antibody molecules would be already deleted during their development in the thymus by a process called Central tolerance – Wikipedia, the key mechanism that ensures our immune system doesn’t constantly attack our own cells, tissues and organs.

Central tolerance though is and never could be complete, no, not even in the healthiest of humans, for the simple reason that not everything that can be expressed by the body (called the periphery by immunologists, as opposed to the thymus where Central Tolerance occurs) is or could be expressed and/or presented by the thymus. This is especially the case for one particular portion of antibodies namely a part within its variable portion.

Antibodies have essentially two parts that help them perform their various functions (which immunologists call effector functions).

Peptides derived from an antibody’s hypermutated region, its CDR3, could not only be antigens but could theoretically also serve as immunogens for T cells. However, this normally rarely happens even in autoimmunity because T cell generation is a Stochastic – Wikipedia process and frequency of T cells with receptors capable of binding peptides derived from any one antibody’s CDR3 are too few to get a full-fledged immune response going.

OTOH, ordinarily an antibody’s constant portion, its FcR, is far less likely to be an immunogen. T cells whose receptors could bind FcR-derived peptides would be deleted during their development in the thymus by the process of Central Tolerance. Thus, antibody’s Fc portion could usually become targets of body’s own immune response only when normal tolerance mechanisms break down, as happens in autoimmunity. This is because as long as they belong to the same isotype (antibody class), a whole bunch of antibodies specific for different antigens would still have the same Fc portion. Thus, provided there is a problem with Central Tolerance, this increases the likelihood of sufficient T cells whose receptors could ‘see’ Fc-derived peptides to initiate and sustain an anti-antibody response.