T and B lymphocytes

Both lineages arise from a common lymphoid progenitor in the bone marrow, then diverge by where they mature. B lymphocytes complete maturation in the bone marrow; T lymphocytes migrate to the thymus, where positive selection retains cells whose receptors recognize self-MHC and negative selection deletes those reacting strongly to self-antigen. Each mature cell carries a uniquely rearranged antigen receptor, giving the adaptive immune system its enormous specificity.

T cells recognize antigen only when it is presented on MHC molecules. CD4⁺ helper T cells read peptides on MHC class II displayed by antigen-presenting cells and coordinate the response by secreting cytokines — Th1 activating macrophages and cytotoxic responses, Th2 supporting antibody and antiparasitic responses. CD8⁺ cytotoxic T cells read MHC class I on any nucleated cell and kill infected or malignant targets. Regulatory T cells restrain the response and maintain tolerance. B cells, by contrast, bind free antigen directly through surface immunoglobulin; with helper T cell signals they undergo class switching and affinity maturation in germinal centers and differentiate into antibody-secreting plasma cells and long-lived memory cells.

The division of labor explains clinical patterns. Defects in T cell function cause susceptibility to viral, fungal, and intracellular infections, while defects in B cell function cause recurrent encapsulated bacterial infections beginning after maternal antibody wanes. Memory in both lineages is what makes vaccination work and why a second exposure produces a faster, stronger response than the first.

USMLE Step 1 immunology tests these cells constantly: the maturation sites, the MHC class I versus class II restriction rule, the CD4 and CD8 surface markers, and the immunodeficiency syndromes that follow from losing either arm. Anchoring the CD4-with-class-II and CD8-with-class-I pairings early makes the rest of the immunology section far easier.