Host defenses were evaluated in 70 healthy aged volunteers. Individuals who had diseases or who were taking medication known to affect the inflammatory and immune responses were excluded from the study. Volunteers were followed for 24 months to correlate their state of health with the evaluation of host defenses. Polymorphonuclear leukocyte function and the serum opsonic capacity for Escherichia coli and Staphylococcus aureus were normal. Assays of complement components and activity revealed unexplained elevations in native C3 and properdin, normal concentrations of factor B, normal conversion of C3 by inulin, and normal levels of hemolytic complement. The levels of IgG and IgA did not differ from levels noted in younger controls, but the concentration of IgM was decreased and that of IgE increased. The prevalence of autoantibodies was low. None of the volunteers were anergic, but lymphocyte responses to mitogens were depressed in three-day cultures. The number and percentages of E-rosette-forming cells and cells bearing surface IgD or IgM were normal. No lymphopenia was noted.

The immune system has evolved in the human being as an elaborate mechanism to distinguish itself from all else that is not self. This process serves in the defence against invaders. The cells of the immune system learn to tolerate all tissues, cells and proteins of the body. Failure to control the state of tolerance results in autoimmunity. The understanding of the role of T-cell receptors (TCR), the Major Histocompatibility Complex (MHC), adhesion molecules and growth factors in antigen recognition has lead to the exploration of various means to modulate the immune response. Safety measures exist to prevent the immune system from attacking its host. The antigen has to be recognized by the T-cell. This involves the TCR and the MHC. In addition it must receive a second signal to become activated. The second signal involves a protein such as B7 binding with CD28. Certain specialized cells, macrophages, dendritic cells and activated B-cells can deliver this second signal for activation; receipt of only one signal can prevent activation. The elucidation of the role of cell-to-cell interactions, the adhesion molecules involved and the accessory growth factors provides modalities for selectively modifying the immune response. This would be of great relevance in autoimmunity and transplantation.

No abstract

No abstract