lymph node

Structurally, a lymph node has an outer cortex containing primary and secondary follicles (with germinal centers) populated by B lymphocytes and follicular dendritic cells; a paracortex containing T lymphocytes and high endothelial venules (HEVs) through which lymphocytes enter from blood; and an inner medulla with medullary cords (plasma cells, macrophages) and medullary sinuses that drain into efferent lymphatics. Afferent lymphatics bring lymph (and antigen) into the subcapsular sinus, where macrophages and dendritic cells sample antigens and present them to T and B cells, initiating adaptive immune responses. Lymph nodes are key sites for class switching and affinity maturation of B cells within germinal centers, a process dependent on T follicular helper cells and CD40L-CD40 interactions (deficiency causes Hyper-IgM syndrome). Clinically, lymphadenopathy is categorized as reactive (infection, autoimmune disease), granulomatous (TB, sarcoidosis, cat-scratch disease), or neoplastic (metastatic carcinoma typically involves subcapsular sinus first; lymphomas cause architectural effacement). Paracortical hyperplasia is seen in viral infections (e.g., EBV) due to T-cell proliferation, whereas follicular hyperplasia occurs in early HIV infection, rheumatoid arthritis. Location-specific lymphadenopathy has diagnostic significance: e.g., Virchow's node (left supraclavicular) suggests abdominal or thoracic malignancy (Trousseau's sign of malignancy is different but linked to same idea), and sentinel lymph node biopsy is used clinically to assess spread of breast cancer and melanoma. Sinus histiocytosis (dilated sinuses with macrophages) is often seen in nodes draining a cancer, especially melanoma. Understanding lymph node histology and pathologic reaction patterns is essential for diagnosing infectious, autoimmune, and neoplastic diseases in pathology and immunology.