Aging and the mucosal-associated lymphoid system

Several lines of evidence support the notion that the mucosal-associated lymphoid system differs from the systemic. It is possible that the mucosal lymphoid system may also differ from the systemic system with regard to immune competence with age. Our findings in these studies indicate a lack of age-associated immune dysfunction in the mucosal-associated lymph nodes: that is, mesenteric and mediastinal lymph node PFC responses of old mice that revealed no decline in magnitude were found to be highly heterogeneous with regard to antibody affinity and revealed no appreciable anti-idiotype-blocked, hapten-augmentable plaque-forming cells. By contrast, the number of splenic and, as well, draining peripheral lymph node IgM, IgG, and IgA anti-TNP PFC responses to TNP-BGG was found to decrease with age with a preferential loss of high affinity plaque-forming cells. This decline in immune activity in the systemic tissues coincided with the increased appearance of anti-idiotype-blocked, hapten-augmentable plaque-forming cells. This differential effect of aging on immune responses in vivo of mucosal and systemic lymphoid tissues imply a site preference for an age-related decline in immune function, and a division of the immune system into regulatory compartments during the normal immune response to antigen in old mice. The present demonstration of a differential effect of aging on immune function in vivo raises an important issue with regard to age-related host defense mechanisms. For example, it would seem reasonable to predict that if immune function totally wanes with age, old individuals would be greatly susceptible to disease and infection. On the contrary, host defense mechanisms relevant to infection show minimal alterations in healthy aged individuals. Thus, we believe that mucosal immunity may play a very important role in host defenses in elderly individuals.