B and T cells are generic terms for families of similar lymphocytes that are the core of adaptive immunity. They are morphologically similar with similar origins, however, have vastly different roles when matured, differentiated, and responding to pathogenic invasion.
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B and T cells share an origin from hematopoietic stem cells which begin to mature and differentiate in the fetal liver during development, and the bone marrow postnatally. T cells mature in the thymus gland whereas B cells mature in the bone marrow primarily but are transported to lymph nodes or the spleen to mature further.
Upon maturation, T cells are transported to lymphoid tissue and are termed “peripheral” T cells, made up of regulatory T cells (Treg), memory T cells (Tmem), and naive T cells. At birth, the majority of peripheral cells are naive T cells, this shifts through development where Tmem eventually becomes the majority. The generation of Tmem plateaus during late adulthood but the population is maintained throughout life.
Rodent models have been used to characterize T cell action into 3 main phases: clonal expansion, contraction, and memory. Clonal expansion is the process where T cells are activated by a pathogen to undergo rapid cell replication and differentiation, this can be done by an antigen-presenting cell (APC) associated with a major histocompatibility complex class II (MHC II) complex.
B cells can act as APCs whereas T cells cannot, and only recognize antigens presented by such cells. Naive T cells can be stimulated to differentiate into effector T cells like T helper (Th) cells, which release a variety of cytokines upon stimulation by an APC to activate B cells and macrophages or cytotoxic T cells (Tc) which induce apoptosis in target pathogens when activated.
When uncontrolled, clonal expansion can be detrimental to host tissue and can result in autoimmunity at worst. Therefore, the colony “contracts”, reducing populations to leave few Tmem which retain a memory of the foreign antigen. The effector cleanup pathway triggers caspases via extrinsic or intrinsic stimulation to induce apoptosis, leaving few Tmem cells within the periphery for the duration of adulthood.
Tmem populations contain subpopulations, a recent discovery is the presence of tissue-resident memory (Trm) cells in humans after the first discovery in rodent tissue. Human Trm is thought to assist in mediating protective responses and maintaining long-term immunity.
B cells are more independent than T cells, the main difference lies in their production of antibodies. Fetal B cells are T-independent which allows immune responses without the need for T cell activation. Fetal B cells, and some postnatal B cells, express “natural” IgM antibodies which mainly maintain tissue homeostasis.
Unlike T cells, postnatal B cells undergo a secondary maturation after primarily differentiating in bone marrow. Sites of secondary maturation include the lymph nodes and the spleen. B cells contribute to T cell activation which triggers a positive feedback loop of B cell activation. B cells are capable of antigen presentation which enables T cell priming and simultaneously allows B cells to signal to allow cell differentiation among B cell populations to plasma and memory cells.
Two subtypes of B cells are named from their site of secondary maturation. Follicular B cells mature in the follicles of the lymphoid organs, their main functions are antigen presentation and T-dependent signaling.
Marginal zone B cells (MZB) are located within the marginal zones of the spleen but also inhabit a variety of lymph nodes and glands, these cells are capable of T-independent responses as well as T-dependent. MZB is highly sensitive to low concentrations of foreign antigens and can differentiate into plasma cells in the presence of IL-2 and IL-10 cytokines.
Memory B cells differentiate from activated B cells and are classified based on their expression profiles among other factors. They are generated upon the conclusion of the immune response as mediated by regulatory B cells. Regulatory B cells act similarly to Treg in the expression of cytokines and chemokines to modulate the inflammatory response and prevent uncontrolled reactions. IL-10 specifically is released to inhibit the release of pro-inflammatory cytokines and encourage the differentiation of T cells into Treg cells.
B and T cells are similar in a variety of ways, both are lymphocytes that are involved in the adaptive immune response and differentiate into memory and regulatory cells. However, they are fundamentally different in their ability to respond to pathogenic insults.
T cells facilitate a primary response and are key in activation of B cells and macrophage recruitment, whereas B cells retain most of the immunological memory, partake in activation, and are more able to respond independently of other cells.
Despite being morphologically indistinct, the functions these cells are capable of are complex and are key to understanding cases wherein these interactions are dysfunctional.
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