Publisher Summary This chapter discusses many observations indicating a decline in immune function with aging both in experimental animals and in humans. It is evident that a decline in T cell function gradually occurs and this affects the entire immune system. Antibody formation and B cell function appear to be secondarily altered. Various autoantibodies are increased in older experimental animals and humans that may relate to the observed decrease in suppressor cells. Cell-mediated immunity has been analyzed in vivo and in vitro. Various T cell-dependent functions decline with age. Normal immune functions can begin to decline as early as when an individual reaches sexual maturity. The decline is due to changes in the immune cells and their milieu. Cell loss, shift in the proportion of subpopulations, and qualitative cellular changes, the three possible types of changes that can cause the decline, have all been detected.

Age influence on the immune system.

Tear physiology and dry eyes.

The oxidative products of arachidonic acid and other mediators of immediate hypersensitivity are released by mast cells and other cells in response to the presence of noxious substances. In a normal response these chemicals produce the local inflammatory reactions that accompany destruction of the noxious substance. When the host response is misdirected or excessive, the concerted action of the same chemical mediators may produce allergic or inflammatory disease.

Mediation of local homeostasis and inflammation by leukotrienes and other mast cell-dependent compounds.

1975 is the fiftieth anniversary of the proposal, by Gorter and Grendel, that biological membranes are based on a lipid bilayer. Now well established, this proposal, like the DNA double helix, was a major breakthrough in molecular cell biology. Here we discuss current concepts about the molecular composition, organisation and behaviour of the plasma membranes of mammalian erythrocytes and nucleated cells.

Mammalian plasma membranes.

The binding of concanavalin A to T but not B mouse spleen lymphocytes increases Ca2+ uptake in these cells which is measurable by 45 s and complete by 1 min. Dibutyryl cyclic AMP, but not sodium azide inhibits induced Ca2+ uptake, whereas dibutyryl cyclic GMP enhances it. B cell mitogens do not cause a similar Ca2+ uptake in mouse B lymphocytes. The induction of increased Ca2+ uptake by T cells is discussed in terms of gated membrane channels for Ca2+.

Induction of increased calcium uptake in mouse T lymphocytes by concanavalin A and its modulation by cyclic nucleotides.

Cyclic AMP, Cell Growth, and the Immune Response

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Papers

Cyclic AMP, Cell Growth, and the Immune Response

Cyclic AMP, cell growth, and the immune response : proceedings of the symposium held at Marco Island, Florida, January 8-10, 1973