Sudden infant death syndrome (SIDS): T-cell immunodeficiency--Part 1.
It is hypothesized that SIDS mimics AIDS and atopic eczema in that defective T lymphocytes and overactive B cells overstimulate pro-inflammatory cytokines in the mucosal immune system. Virally infected cells are unable to convert linoleic acid (LA) into gamma-linolenic acid (GLA) which eventually leads to defective T lymphocyte production. Abnormal lung cytokine synthesis by virus-induced immunodeficient T lymphocytes is associated with the murine AIDS-related complex (ARC). Adenosine triphosphate (ATP) deficient anaerobic cells cannot convert LA to GLA. It is hypothesized that, in SIDS victims, elevated levels of hypoxanthine and immunoglobulins are evidence of chronic hypoxemia and ATP catabolism, and an inability to convert LA to GLA, leading to defective T lymphocytes in the mucosal immune system.
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D044943:Fatty Acid Desaturases / Q000378:metabolism; D005228:Fatty Acids, Essential / Q000378:metabolism; D006801:Humans; D007231:Infant, Newborn; D050602:Linoleoyl-CoA Desaturase; D013398:Sudden Infant Death / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D005228:Fatty Acids, Essential; D044943:Fatty Acid Desaturases; D050602:Linoleoyl-CoA Desaturase