Glossary of terms related to B-cell immune responses
| Term . | Definition . |
|---|---|
| AID (AICDA) | Enzyme responsible for driving the somatic hypermutation and class switch recombination mechanisms in activated B cells, both of which contribute to B-cell receptor diversification. |
| Affinity maturation | Process by which GCBs develop B-cell receptors with increased antigen affinity through repeated rounds of diversification, competitive selection, and clonal expansion. |
| Anergy | Condition in which mature B cells persist in periphery but are poorly responsive to antigen, responsible for silencing self-reactive B cells. Anergy loss contributes to autoimmune disorders. |
| Antigen or molecular mimicry | Phenomena in which sequence similarities between foreign and self-antigens are sufficient to result in the cross-activation of auto-reactive B cells by pathogen-derived antigens. |
| Antigen presentation | Surveillance process, essential for T-cell activation, in which T cells screen short peptide antigens displayed on the surface of other cells. |
| B-cell receptor | Membrane-bound immunoglobulin-type receptor, acquired early during B-cell development, that recognizes and binds specific antigens causing activation of mature B cells. |
| B-cell receptor or antibody repertoire | Collection of B-cell receptors/immunoglobulin sequences expressed by a given population of B cells. |
| Class switch recombination/isotype switching | DNA recombination process by which the B-cell receptor constant portion is exchanged in mature activated B cell, generating functional diversity while maintaining antigen specificity. |
| Clonal precursor cells | Genetically distinct subpopulations of B cells thought to clonally derive from a single founding cell which, following acquisition of one or more somatic mutations, gained a disproportionate proliferative advantage over other mature B-cell populations. |
| Follicular dendritic cells | Nonhematopoietic stromal cells in B-cell follicles and GCs that retain antigens at their cell surface in a manner crucial to the selection of B cells expressing high-affinity antigen receptors. |
| Germinal center reaction | Transient immune structures formed in lymphoid organs, in which activated B cells proliferate, mutate their B-cell receptors, and differentiate to generate high-affinity antibodies and immunological memory. |
| Immune synapse | Specialized cell–cell junction between T cells and antigen-presenting cells, such as GCBs, that allows focal mutual interaction via soluble and membrane-bound factors. |
| Off-target mutations | Also known as aberrant somatic hypermutation (aSHM). Sporadic mutations introduced by AID in loci beyond the B-cell receptor, as a byproduct of the somatic hypermutation mechanism in activated B cells. |
| Recall response | Adaptive immune reaction mounted by memory B cells on re-encounter with identical or closely related antigenic challenges. These secondary responses tend to be faster and enhanced compared with original/primary immune responses. |
| Self-reactivity | Recognition of autologous antigens by a B-cell receptor, potentially capable of evoking a pathogenic immune response by the host. |
| Somatic hypermutation | Mechanism of B-cell receptor sequence diversification through locus-directed DNA mutagenesis, catalyzed by the enzyme AID in activated mature B cells. |
| T-follicular helper cells | Specialized subset of CD4+ T-cells essential for GC formation and maintenance, affinity maturation, and development of most high-affinity antibodies and memory B cells. |
| Term . | Definition . |
|---|---|
| AID (AICDA) | Enzyme responsible for driving the somatic hypermutation and class switch recombination mechanisms in activated B cells, both of which contribute to B-cell receptor diversification. |
| Affinity maturation | Process by which GCBs develop B-cell receptors with increased antigen affinity through repeated rounds of diversification, competitive selection, and clonal expansion. |
| Anergy | Condition in which mature B cells persist in periphery but are poorly responsive to antigen, responsible for silencing self-reactive B cells. Anergy loss contributes to autoimmune disorders. |
| Antigen or molecular mimicry | Phenomena in which sequence similarities between foreign and self-antigens are sufficient to result in the cross-activation of auto-reactive B cells by pathogen-derived antigens. |
| Antigen presentation | Surveillance process, essential for T-cell activation, in which T cells screen short peptide antigens displayed on the surface of other cells. |
| B-cell receptor | Membrane-bound immunoglobulin-type receptor, acquired early during B-cell development, that recognizes and binds specific antigens causing activation of mature B cells. |
| B-cell receptor or antibody repertoire | Collection of B-cell receptors/immunoglobulin sequences expressed by a given population of B cells. |
| Class switch recombination/isotype switching | DNA recombination process by which the B-cell receptor constant portion is exchanged in mature activated B cell, generating functional diversity while maintaining antigen specificity. |
| Clonal precursor cells | Genetically distinct subpopulations of B cells thought to clonally derive from a single founding cell which, following acquisition of one or more somatic mutations, gained a disproportionate proliferative advantage over other mature B-cell populations. |
| Follicular dendritic cells | Nonhematopoietic stromal cells in B-cell follicles and GCs that retain antigens at their cell surface in a manner crucial to the selection of B cells expressing high-affinity antigen receptors. |
| Germinal center reaction | Transient immune structures formed in lymphoid organs, in which activated B cells proliferate, mutate their B-cell receptors, and differentiate to generate high-affinity antibodies and immunological memory. |
| Immune synapse | Specialized cell–cell junction between T cells and antigen-presenting cells, such as GCBs, that allows focal mutual interaction via soluble and membrane-bound factors. |
| Off-target mutations | Also known as aberrant somatic hypermutation (aSHM). Sporadic mutations introduced by AID in loci beyond the B-cell receptor, as a byproduct of the somatic hypermutation mechanism in activated B cells. |
| Recall response | Adaptive immune reaction mounted by memory B cells on re-encounter with identical or closely related antigenic challenges. These secondary responses tend to be faster and enhanced compared with original/primary immune responses. |
| Self-reactivity | Recognition of autologous antigens by a B-cell receptor, potentially capable of evoking a pathogenic immune response by the host. |
| Somatic hypermutation | Mechanism of B-cell receptor sequence diversification through locus-directed DNA mutagenesis, catalyzed by the enzyme AID in activated mature B cells. |
| T-follicular helper cells | Specialized subset of CD4+ T-cells essential for GC formation and maintenance, affinity maturation, and development of most high-affinity antibodies and memory B cells. |