T cells differentiate in the thymus and then circulate in the peripheral blood, where they are the principal effec tors of cell-mediated immunity. They also function as helper and suppressor cells, by modulating the immune response through their effect on В cells, plasma cells, macrophages, and other T Cells.
В cells differentiate in bone marrow and possibly in the gut-associated lymphatic tissues (GALT). They are the principal mediators of humoral immunity through their production of antibodies. Once activated by contact with an antigen, they differentiate into plasma cells, which synthesize antibodies that are secreted into the blood, intercellular fluid, and lymph. В lymphocytes also give rise to memory cells, which differentiate into plas ma cells only after the second exposure to the antigen. They are responsible for the secondary, or amnestic response that occurs when the body is exposed to an antigen for a second time. Monocytes vary in diameter from 15-18 mm and are the largest of the peripheral blood cells. They constitute 3-7% of leukocytes.
Monocytes possess an eccentric U-shaped or kidney-shaped nucleus. The cytoplasm has a ground-glass appearance and fine azurophi-lic granules.
Their nuclei stain lighter than lymphocyte nuclei because of their loosely arranged chromatin.
Monocytes are the precursors for members of the mononuclear phagocyte system, including tissue macrophages (histiocytes), osteoclasts, alveolar macrophages, and Kupffer cells of the liver.
Platelets (thromboplastids) are 2-3 mm in diameter.
They are a nuclear, membrane-bound cellular fragments derived by cytoplasmic fragmentation of giant cells, called megakaryocytes, in the bone marrow.
They have a short life span of approximately 10 days.
There are normally 150 000-400 000 platelets per mm>3 of blood. Ultrastructurally, platelets contain two portions: a peripheral, light-staining hyalomere that sends out fine cytoplasmic processes, and a central, dark-staining granulomere that con tains mitochondria, va-cuoles, glycogen granules, and granules. Platelets seal minute breaks in blood vessels and maintain endothelial integrity by adhering to the damaged vessel in a process known as platelet aggregation. Platelets are able to form a plug at the rupture site of a vessel because their mem brane permits them to agglutinate and adhere to surfaces.
Platelets aggregate to set up the cascade of enzymatic reac tions that convert fibrinogen into the fibrin fibers that make up the clot.
