adaptive immunity

Adaptive (acquired) immunity contrasts with innate immunity by being antigen-specific and improving with repeated exposure. It comprises two main branches: humoral immunity, mediated by B lymphocytes that differentiate into plasma cells secreting antigen-specific antibodies (IgM, IgG, IgA, IgE), and cell-mediated immunity, mediated by T lymphocytes (CD4+ helper T cells and CD8+ cytotoxic T cells).

Key processes: Antigen-presenting cells (dendritic cells, macrophages, B cells) process and present antigen via MHC class I (to CD8+ T cells) or MHC class II (to CD4+ T cells). Naïve T cells require two signals for activation: TCR-MHC/peptide binding (signal 1) and costimulation via CD28-B7 (signal 2). CD4+ helper T cells differentiate into subsets (Th1, Th2, Th17, Treg) that orchestrate different immune responses via cytokine secretion. CD8+ cytotoxic T cells kill infected or abnormal cells via perforin/granzyme and Fas-FasL pathways.

B cells recognize antigen via surface immunoglobulin (BCR), undergo somatic hypermutation and class switching (with T cell help via CD40-CD40L interaction) in germinal centers to produce high-affinity antibodies. This process generates immunologic memory—memory B and T cells persist long-term, allowing faster, stronger secondary responses upon re-exposure (basis for vaccination).

Clinical significance: Defects in adaptive immunity underlie primary immunodeficiencies (e.g., SCID—T and B cell defects; DiGeorge syndrome—T cell defect from thymic aplasia; X-linked agammaglobulinemia—B cell defect; hyper-IgM syndrome—CD40L defect impairing class switching). Adaptive immunity is also central to transplant rejection, autoimmune disease pathogenesis, and vaccine design (live attenuated vs. subunit vaccines eliciting different adaptive responses).