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Epitheloid germinal centers: an acquired immunologic deficit?
The histologic structure of lymphoid tissue in cases of fatal infection was reviewed, and epithelioid germinal centers, completely devoid of the usual dark zone of rapidly dividing blast cells, were found in 16 infants and children, one of whom also had Reye's syndrome. Epithelioid change has been previously reported to occur in various childhood infections and in the sudden infant death syndrome. All reported cases have been fatal. In four additional cases there was toxic follicle alteration, or massive necrosis of germinal center cells. Toxic follicle alteration and epithelioid change have been found in childhood infections and sudden infant death syndrome, and some evidence of a pathogenetic relationship between the two was found in this study. It is concluded that epithelioid change represents a definite pathologic alteration of germinal centers associated with total destruction of a whole population of cells. It probably represents an acutely acquired immunologic deficit and therefore may well contribute to the thus far uniformly fatal outcome of the associated diseases.
The histologic structure of lymphoid tissue in cases of fatal infection was reviewed, and epithelioid germinal centers, completely devoid of the usual dark zone of rapidly dividing blast cells, were found in 16 infants and children, one of whom also had Reye's syndrome. Epithelioid change has been previously reported to occur in various childhood infections and in the sudden infant death syndrome. All reported cases have been fatal. In four additional cases there was toxic follicle alteration, or massive necrosis of germinal center cells. Toxic follicle alteration and epithelioid change have been found in childhood infections and sudden infant death syndrome, and some evidence of a pathogenetic relationship between the two was found in this study. It is concluded that epithelioid change represents a definite pathologic alteration of germinal centers associated with total destruction of a whole population of cells. It probably represents an acutely acquired immunologic deficit and therefore may well contribute to the thus far uniformly fatal outcome of the associated diseases.