Final answer:
Pathogen-specific activation of B and T cells leads to the production of effector cells for immediate infection combat and memory cells for long-term immunity. Memory cells enable a rapid and potent secondary immune response if re-exposure to the same pathogen occurs, sometimes preventing the establishment of an infection without the individual's awareness.
Step-by-step explanation:
Activation of pathogen-specific B and T cells not only provides effector cells for the short-term fight against ongoing infection but also produces memory cells. Plasma B cells produce antibodies to combat pathogens, whereas memory B cells retain the information about the pathogen for future responses. If the individual is re-exposed to the same pathogen, these memory cells can rapidly differentiate into plasma cells and cytotoxic T lymphocytes (CTLs) without the need for antigen-presenting cells (APCs) or helper T (TH) cells, leading to a quicker and more potent secondary immune response.
During a primary immune response, a subset of B and T cells differentiates into memory cells, which do not become effector cells but are primed to do so upon subsequent exposure to the same pathogen. This process is known as immunological memory. These memory B cells can output significantly higher amounts of antibodies than during the primary response, potentially stopping reinfection before it establishes, sometimes without the individual even realizing they have been exposed.
Over time, if the pathogen is not encountered again, these memory cells may decline in number, but they can persist for years or even decades, providing lasting immunity against the pathogen.