LEGEND: The two panels of this chart illustrate the working models of the alternative antigen transport pathway in young and aged mice. These cartoons were based on presently available data. For references on the transport path in old mice click the reference buttons below the legend. It is essential for the viewer to be familiar with the chart presented under the heading Humoral Immune Response, The Alternative Antigen Transport Pathway (See front page of this website). A brief interpretation of the observed age-related changes is the following: Since antigen transport is for the most part defective (e.g., antigen transport cells become phagocytic rather than become transporters of antigens from the afferent lymph to the follicles in the lymph node cortex ) very little antigen is retained on the dendrites of FDCs in the follicles. FDCs also become atrophic and do not develop the normal numbers of dendrites that are typically seen on FDCs from young individuals. Consequently, no iccosomes are produced which typically function in delivering antigen for endocytosis to germinal center B cells. This results in reduced numbers of germinal centers where B memory cells are formed. Therefore, very few B memory cells develop. This will lead to a deficit in antibody secreting plasma cells which begin their development in germinal centers and migrate to the medullary cords of lymph nodes and then to the bone marrow for antibody production. Since the old system is deficient in these plasma cells no feedback occurs and the cycling of the alternative antigen transport pathway is disrupted. The result is a seriously depressed, if not absent, anamnestic immune response. In other words the system thought to be functional in maintaining immunity became defective with aging.