The work in this thesis tests the hypothesis that SIDS infants suffer an abnormal immunological reaction prior to death which results in respiratory obstruction and fatal hypoxia. The triggering factor for this reaction is likely to be a common bacterial or viral antigen. The inflammatory cell population within the pulmonary parenchyma of cases of SIDS, non-pulmonary death controls and pneumonia deaths, has been characterised by immunocytochemistry on paraffin wax embedded tissue sections and snap-frozen tissue. Examination of paraffin wax embedded tissue revealed a significant increase in the pulmonary parenchyma of eosinophils, CD3+ T cells, CD20+ B cells and mast cells compared to deaths from non-pulmonary causes. Neutrophil numbers were significantly reduced in SIDS cases. Analysis of frozen tissue revealed similar results with an increase also in the numbers of CD4+ and CD8+ T cells. There was no significant expansion of any of the variable ( chains and only a small increase in the levels of expression of the ( T cell receptor. Immunocytochemical analysis of the cytokine profile in the pulmonary parenchyma revealed a higher number of cells storing the cytokines Interleukin-4 (IL-4), IL-5, IL-8, IL-10, IL-13 and tumour necrosis factor-( in SIDS cases, but similar numbers of cells storing IL-1(, IL-2, IL-12 as controls. Serum analysis demonstrated a significant increase in the concentration of mast cell tryptase and eosinophil cationic protein, but only a small increase in the concentration of cotinine, whilst mast cell ultrastructural analysis revealed no evidence for anaphylactic-type degranulation. The increased levels of eosinophils, mast cells, B cells and T cells show that there is an inflammatory infiltrate in the lungs of SIDS victims at death. This is probably controlled by the CD4 helper T cell and the release of cytokines which fit the Th2 cytokine profile.