PubMed · 2842477
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N Raab-Traub, K Flynn, C Klein, G Pizza, C De Vinci, L Occhiuzzi, G Farneti, U Caliceti, E Pirodda. 1987. EBV associated malignancies.. https://pubmed.ncbi.nlm.nih.gov/2842477/
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NK cells play an important immunoregulatory role in first line defense mechanisms against infection. As disease progresses, HIV-1 infected patients show loss of NK cytotoxic function, down-modulation and/or loss of expression of both CD16 and CD56 surface Ags on NK cells and a gradual loss of both CD4+ T cells and NK cell numbers. A potential mechanism by which these manifestations may occur in vivo was investigated. We hypothesized that NK-mediated Ab-dependent cellular cytotoxicity (ADCC), using gp120-coated CD4+ peripheral T lymphocytes as targets and anti-HIV serum, will result in the concomitant killing of the CD4+ T lymphocyte targets and the NK lymphocytes. This hypothesis was examined in an in vitro model system. The findings demonstrate that gp120-coated peripheral T lymphocytes can serve as targets and are killed in ADCC. Further, the NK cells that recover from the ADCC reaction show a loss of cytotoxic function, acquire the CD16(dim/-) CD56(dim/-) phenotype and a significant fraction is killed by activation-induced cell death or apoptosis. These findings are reminiscent of the properties of circulating NK cells in HIV-infected patients. The implication of these findings in the pathogenesis of AIDS is discussed.
BACKGROUND: Complications of the biliary anastomosis are the principal cause of clinically serious bacterial sepsis in liver transplant recipients. Reported series suggest an association of bacterial and fungal infection with cytomegalovirus (CMV) infection, although the mechanism of this association is unclear. METHODS: We examined the association of serious bacterial sepsis with CMV replication in a cohort of 106 consecutive liver transplant recipients. Sequentially collected buffy coats were examined with a polymerase chain reaction (PCR) assay that has been shown to have good predictive value for the development of CMV infection. For selected patients, CMV-specific IgM response and serum tumor necrosis factor-alpha (TNF-alpha) were also measured. RESULTS: Ten of 13 patients with serious bacterial sepsis developed buffy coat PCR positivity, compared with 26 of 93 patients without bacterial sepsis (chi-square, P<0.001). Ten of 10 septic recipients with a seropositive liver donor developed PCR positivity. For 9 of 10 recipients, bacterial sepsis developed before PCR positivity. Bacterial sepsis was associated with high serum levels of TNF-alpha. Immune response to CMV (reflected by the appearance CMV-specific IgM) was apparently affected by bacterial sepsis, and IgM response was not observed for the three septic patients who died during the study period. CONCLUSIONS: We conclude that CMV replication is encouraged by serious bacterial sepsis. Replication may be promoted by high antecedent levels of TNF-alpha, and/or by poor immune response to CMV in the context of serious bacterial infection.
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