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white pulp

Histology / ImmunologyHematologic/LymphaticImmune

Summary

White pulp is the lymphoid (immune) component of the spleen, consisting of the periarteriolar lymphoid sheath (PALS, T cells), lymphoid follicles (B cells), and the marginal zone. It surrounds the central arteries and mediates immune responses to blood-borne antigens, particularly encapsulated organisms.

Detail

**Structure (spleen histology):** - **Central arteriole** (branch of the trabecular artery) is surrounded by: - **PALS (periarteriolar lymphoid sheath):** T cells (CD4+ and CD8+); T-cell zone. - **Lymphoid follicles:** B cells; primary follicles are inactive, secondary follicles have germinal centers after antigen stimulation. Follicles sit eccentrically on the PALS, so the central arteriole appears off-center. - **Marginal zone:** the interface between white and red pulp. It contains macrophages, dendritic cells, and specialized marginal zone B cells. Blood-borne antigens are filtered and captured here, and APCs present them to lymphocytes. - White pulp makes up about 25% of splenic tissue. Red pulp (splenic cords of Billroth and venous sinusoids) makes up the rest and handles RBC filtration and removal of old or damaged RBCs.

**Function:** - Immune surveillance of blood: antigen capture and presentation, B-cell activation, and plasma cell and antibody production. - Marginal zone B cells and macrophages are key for responses to **encapsulated bacteria** (S. pneumoniae, H. influenzae type b, N. meningitidis). These are T-independent polysaccharide antigens, and the marginal zone is the main site of response. - Opsonized bacteria are cleared by splenic macrophages.

**Clinical correlations:** - **Asplenia/hyposplenism** (splenectomy, sickle cell autosplenectomy) causes loss of white pulp function. This leads to risk of overwhelming post-splenectomy infection (OPSI) from encapsulated organisms. Give vaccines against pneumococcus, Hib, and meningococcus, ideally ≥2 weeks before elective splenectomy. - **Lab findings after splenectomy:** Howell-Jolly bodies (nuclear remnants), target cells, Heinz bodies, and thrombocytosis and lymphocytosis. - **Hyposplenism:** red pulp dysfunction causes failure to remove RBC inclusions; white pulp loss causes immune deficiency. - **B-cell deficiencies** (e.g., X-linked agammaglobulinemia) show absent or underdeveloped follicles and germinal centers. **T-cell deficiencies** (e.g., DiGeorge syndrome) show depleted PALS. - **Splenic lymphoma/neoplasia:** splenic marginal zone lymphoma arises from marginal zone B cells and expands the white pulp. It is associated with HCV and presents with splenomegaly. - **Gross pathology:** in amyloidosis, "sago spleen" (deposition in the white pulp, producing a tapioca-like appearance) contrasts with "lardaceous spleen" (red pulp involvement). - **Infection or immune stimulation:** reactive follicular hyperplasia enlarges the white pulp. Examples include sepsis, infectious mononucleosis, and acute splenitis.

**High-yield contrast:** - **White pulp:** immune function (T and B cells). - **Red pulp:** RBC filtration and storage, as well as hematopoiesis in extramedullary hematopoiesis. It is the site of destruction in hereditary spherocytosis and ITP.

**Mnemonic:** White = Lymphocytes (immune, "white" blood cells); Red = RBCs.

Sources

  • First Aid for the USMLE Step 1 (Immunology: Lymphoid structures; Hematology)
  • Robbins & Cotran Pathologic Basis of Disease (Spleen)
  • Junqueira's Basic Histology (Lymphoid Organs)
  • Costanzo Physiology / Abbas Cellular and Molecular Immunology
  • Pathoma (Fundamentals of Pathology) – Hematopathology

Reviewed by Medusa editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.