L5 Flashcards
Clonal deletion
Process where self-reactive immature B cells in the bone marrow undergo apoptosis
Receptor editing
Rearrangement of light chain genes in B cells to avoid self-reactivity
Hematopoietic Stem Cells (HSCs)
Multipotent stem cells in bone marrow capable of self-renewal and giving rise to all blood cell types
Common Lymphoid Progenitors (CLPs)
Progenitor cells derived from HSCs that give rise to B cells, T cells, and NK cells
Follicular dendritic cells (FDCs)
Retain antigens on their surface in germinal centers to select B cells with high-affinity receptors
V(D)J recombination
Process during B-cell development combining variable, diversity, and joining segments to generate diversity
Junctional diversity
Addition or deletion of nucleotides at V-D-J junctions, increasing antibody variability
Somatic hypermutation (SHM)
Mutations introduced in antibody variable regions after B-cell activation to improve antigen affinity
Class-switch recombination (CSR)
Process allowing B cells to change antibody isotype while maintaining antigen specificity
Activation-induced cytidine deaminase (AID)
Enzyme crucial for somatic hypermutation and class-switch recombination
IFN-γ
Cytokine promoting IgG production and Th1 responses
IL-4
Cytokine inducing IgE class switching
TGF-β
Cytokine promoting IgA class switching and immune tolerance
Hyper IgM syndrome
Condition caused by defects in CD40 or CD40L, impairing isotype switching and leading to high IgM levels
Naive B cells
Mature B cells that have not yet encountered their specific antigen
Plasma cells
Differentiated B cells that produce large quantities of antibodies
Memory B cells
Long-lived B cells that rapidly respond to re-exposure to their specific antigen
T-dependent B-cell responses
Require T cell help and involve germinal center formation, affinity maturation, and memory development
T-independent B-cell responses
Do not require T cell help and primarily produce low-affinity IgM antibodies
Somatic hypermutation
Occurs in germinal centers, introducing mutations to enhance antibody affinity but may cause self-reactivity
Neutralization
Antibody-mediated mechanism preventing pathogens or toxins from binding to host cells
Opsonization
Process where antibodies coat pathogens, enhancing their phagocytosis by immune cells
Complement activation
Antibody-mediated activation of the complement cascade leading to pathogen lysis or inflammation