“…This histological response requires 1-2 weeks after exposure to antigen and has been observed in perinatal autopsies of infants who have persistent viral infections established prior to birth or in the early neonatal period. [11][12][13][14][15] GC and mature plasma cells were reported in a significant minority of autopsies of fetuses with congenital rubella syndrome suggesting that the immune system of a normal human fetus, as early as the late second trimester of gestation, is competent to respond with histological features of an acquired humoral immune response. Such direct observations in human fetuses are augmented by the recent demonstration that in the second trimester, the lymphoid tissues of the rhesus monkey fetus have a complete repertoire of properly organized antigen-presenting cells, T cells, and B cells.…”
We hypothesized that if infection is the proximate cause of congenital biliary atresia, an appropriate response to antigen would occur in lymph nodes contiguous with the biliary remnant. We compared the number of follicular germinal centers (GC) in 79 surgically excised hilar lymph nodes (LN) and 27 incidentally discovered cystic duct LNs in 84 subjects at the time of hepatic portoenterostomy (HPE) for biliary atresia (BA) to autopsy controls from the pancreaticobiliary region of non-septic infants >3 months old at death. All 27 control LN lacked GC, a sign in infants of a primary response to antigenic stimulation. GC were found in 53% of 106 LN in 56 of 84 subjects. Visible surgically excised LN contiguous with the most proximal biliary remnants had 1 or more well-formed reactive GC in only 26/51 subjects. Presence of GC and number of GC/LN was unrelated to age at onset of jaundice or to active fibroplasia in the biliary remnant but was related to older age at HPE. Absent GC in visible and incidentally removed cystic duct LNs predicted survival with the native liver at 2 and 3 years after HPE, P = .03, but significance was lost at longer intervals. The uncommon inflammatory lesions occasionally found in remnants could be secondary either to bile-induced injury or secondary infection established as obstruction evolves. The absence of consistent evidence of antigenic stimulation in LN contiguous with the biliary remnant supports existence of at least 1 major alternative to infection in the etiology of biliary atresia.
“…This histological response requires 1-2 weeks after exposure to antigen and has been observed in perinatal autopsies of infants who have persistent viral infections established prior to birth or in the early neonatal period. [11][12][13][14][15] GC and mature plasma cells were reported in a significant minority of autopsies of fetuses with congenital rubella syndrome suggesting that the immune system of a normal human fetus, as early as the late second trimester of gestation, is competent to respond with histological features of an acquired humoral immune response. Such direct observations in human fetuses are augmented by the recent demonstration that in the second trimester, the lymphoid tissues of the rhesus monkey fetus have a complete repertoire of properly organized antigen-presenting cells, T cells, and B cells.…”
We hypothesized that if infection is the proximate cause of congenital biliary atresia, an appropriate response to antigen would occur in lymph nodes contiguous with the biliary remnant. We compared the number of follicular germinal centers (GC) in 79 surgically excised hilar lymph nodes (LN) and 27 incidentally discovered cystic duct LNs in 84 subjects at the time of hepatic portoenterostomy (HPE) for biliary atresia (BA) to autopsy controls from the pancreaticobiliary region of non-septic infants >3 months old at death. All 27 control LN lacked GC, a sign in infants of a primary response to antigenic stimulation. GC were found in 53% of 106 LN in 56 of 84 subjects. Visible surgically excised LN contiguous with the most proximal biliary remnants had 1 or more well-formed reactive GC in only 26/51 subjects. Presence of GC and number of GC/LN was unrelated to age at onset of jaundice or to active fibroplasia in the biliary remnant but was related to older age at HPE. Absent GC in visible and incidentally removed cystic duct LNs predicted survival with the native liver at 2 and 3 years after HPE, P = .03, but significance was lost at longer intervals. The uncommon inflammatory lesions occasionally found in remnants could be secondary either to bile-induced injury or secondary infection established as obstruction evolves. The absence of consistent evidence of antigenic stimulation in LN contiguous with the biliary remnant supports existence of at least 1 major alternative to infection in the etiology of biliary atresia.
“…Ffir die Insuffizienz des T-Zellsystems -als endogener pathogenetischer Faktor -k6nnte eine Altersatrophie des lymphatischen Systems [12], aber auch eine virale Ursache verantwortlich sein. Speziell von R6telnviren ist bekannt, dab sie unter bestimmten Voraussetzungen zu einer persistierenden Infektion ffihren und neben anderen Zellen auch Lymphozyten und Thymozyten infizieren [21][22][23], ferner dab sie die PHA-Aktivit/it der Lymphozyten hemmen [21] und in der Zellkultur Chromosomenverfinderungen hervorrufen und die Zellteilung blockieren [18].…”
The presence of rubella virus antigen was demonstrated by means of immunohistological methods in two cases of angioimmunoblastic lymphadenopathy. One patient had elevated serum anti rubella titer and myocarditis. These findings support the idea that angioimmunoblastic lymphadenopathy develops as a combined effect of persistent virus infection and partial immune deficiency.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.