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http://www.journals.uchicago.edu/JID/journal/issues/v188n3/30081/brief/30081.abstract.html

The Journal of Infectious Diseases    2003;188:433-439
© 2003 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2003/18803-0013$15.00

 


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MAJOR ARTICLE

Differences in Participation of Innate and Adaptive Immunity to Respiratory Syncytial Virus in Adults and Neonates

Subramaniam Krishnan,1,4 Mary Craven,4 Robert C. Welliver,5 Nafees Ahmad,3 and Marilyn Halonen2,3,4

1Graduate Program in Microbiology and Immunology, Departments of 2Pharmacology and 3Microbiology and Immunology, and 4Arizona Respiratory Center, University of Arizona Health Sciences Center, Tucson; 5Department of Pediatrics, State University of New York at Buffalo

 

Received 18 September 2002; accepted 3 March 2003; electronically published 10 July 2003.

Innate and adaptive immune responses to respiratory syncytial virus (RSV) in neonates were assessed by cord blood mononuclear cell (MC) cytokine expression and proliferation and these responses were compared with those from adult peripheral blood MCs. In adult cells, inactivated and live virus invoked cytokines reflecting both innate and adaptive immunity (interleukin [IL]–6, interferon [IFN]–γ, IL-2, tumor necrosis factor [TNF]–α, and IL-10). Low levels of IL-4 were detected, although only with inactivated virus. In contrast, in neonatal cells, inactivated virus invoked large levels of the innate immune cytokines IL-6, TNF-α, and IL-10 and reduced levels of IFN-γ and IL-12 but no adaptive cytokines. Live virus induced fewer innate (IL-6, IL-10, and IFN-γ) and no adaptive immune cytokines. RSV-induced proliferation was absent in neonatal MCs, although positive in adult MCs. Thus, exposure to RSV does not appear to occur before birth, and adaptive immune insufficiency or greater innate responses may account for early life RSV-induced illnesses.

 



     Presented in part: American Academy of Allergy, Asthma and Immunology (AAAAI), New Orleans, 16–21 March 2001 (abstract 311); AAAAI, San Diego, 3–8 March 2000 (abstract 887).
     Financial support: National Institutes of Health (grants AI-44697, P50 HL 67672, and AI-42268).

 

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