B cells, or B lymphocytes, are white blood cells and a central component of the adaptive immune system. Their main function is to generate specific antibodies, which are specialized proteins that neutralize threats like bacteria, viruses, and toxins. This process, termed humoral immunity, is essential for defense against pathogens existing outside of host cells. When a B cell encounters a foreign substance, or antigen, it undergoes activation and differentiation to launch a highly targeted immune response, fighting current infections and establishing long-lasting protection.
Recognizing the Threat and Initiating the Response
The B cell response begins with the recognition of an invader through the B Cell Receptor (BCR), a membrane-bound antibody molecule on the cell surface. Each B cell has a unique BCR that binds to one specific antigen shape, ensuring a highly selective response. Upon binding the antigen, the receptor-antigen complex is pulled inside the cell via endocytosis.
Once internalized, the pathogen material is broken down into peptide fragments. These fragments are loaded onto Major Histocompatibility Complex Class II (MHC Class II) molecules. The B cell, now an antigen-presenting cell, displays this MHC-antigen complex on its surface. This presentation is necessary for the most robust activation, which is dependent on Helper T cells. Helper T cells specific for the same antigen recognize this presentation, linking the two arms of the adaptive immune system.
This interaction is a two-signal system. Antigen binding to the BCR is the first signal, and the Helper T cell provides the second, co-stimulatory signal. The T cell engages the B cell through surface molecules like CD40L and CD40, and releases chemical messengers called cytokines. These cytokines drive the B cell to activate, proliferate rapidly, and differentiate.
T-Independent Activation
A less common pathway, T-independent activation, occurs when a B cell encounters antigens with highly repetitive structures, such as those on bacterial capsules. These antigens directly cross-link multiple BCRs, activating the B cell without T cell help. This response is limited, producing lower-affinity IgM antibodies and failing to generate long-term immune memory.
The Antibody Factory: Plasma Cells and Effector Function
Following activation, the B cell undergoes massive clonal expansion, multiplying rapidly to create a large population of identical cells. This proliferation generates the necessary fighting power to overcome the infection quickly. The B cells then differentiate into specialized antibody-secreting cells known as plasma cells.
Plasma cells are terminally differentiated and no longer divide, instead devoting their machinery to protein synthesis. They increase internal structures, particularly the rough endoplasmic reticulum, to facilitate the enormous production of antibodies. A single plasma cell can secrete up to 2,000 antibody molecules per second. These soluble antibodies circulate throughout the body, seeking the specific pathogen that triggered their production.
Antibodies are Y-shaped proteins. The two arms contain variable regions that bind precisely to the target antigen, while the tail determines the antibody’s class and effector function.
Antibody Effector Functions
- Neutralization: Antibodies physically coat the pathogen or toxin, preventing it from binding to and infecting host cells.
- Opsonization: The antibody acts as a flag, coating the microbe to make it more visible for immune scavenger cells like macrophages to engulf and destroy.
- Complement Activation: Antibodies can trigger the complement cascade, resulting in the direct lysis, or bursting, of the bacterial cell wall.
Many plasma cells are short-lived, serving to clear the immediate infection. The volume of antibodies they produce provides the rapid, protective flood necessary to control the invading pathogen.
Creating Lasting Protection: Immune Memory
The strongest B cell response, leading to long-term protection, occurs within specialized microenvironments in the lymph nodes called germinal centers.
Affinity Maturation
In these centers, somatic hypermutation introduces small, random changes into the genes coding for the antibody’s variable region. B cells whose mutations result in a BCR that binds the antigen more tightly are preferentially selected to survive and proliferate. This process, known as affinity maturation, ensures that later antibodies are more potent than the initial ones.
Class Switching
B cells simultaneously undergo Class Switching (Isotype Switching), changing the antibody’s constant region while retaining the high-affinity variable region. This allows the B cell to switch from producing the early-response antibody IgM to other classes, such as IgG, IgA, or IgE, which are suited for different locations and functions. For example, IgG is abundant in blood, IgA is secreted onto mucosal surfaces, and IgE is involved in allergic responses.
The germinal center reaction generates two types of long-lived cells that confer immune memory:
- Memory B Cells: These dormant, specialized cells circulate for decades. Upon re-exposure to the pathogen, they rapidly activate, bypassing initial steps and quickly differentiating into plasma cells. This accelerated secondary response is the basis of successful vaccination.
- Long-Lived Plasma Cells: These cells migrate to protective niches, primarily in the bone marrow. They persist for years, continuously secreting low levels of high-affinity antibodies into the bloodstream. This constant circulation provides a sustained barrier against reinfection.