title: Impaired T cell proliferation in acute dengue infection.
abstract: Decreased proliferative responses to mitogens and recall Ags have been observed in PBMC obtained during several acute human viral infections. To determine whether cell-mediated responses are altered during acute dengue infection, we examined the proliferative responses of PBMC from children enrolled in a prospective study of dengue infections in Thailand. All responses of PBMC during acute illness were compared with the same patients' PBMC obtained at least 6 mo after their infection. Proliferative responses to PHA, anti-CD3, tetanus toxoid, and dengue Ags were decreased significantly in PBMC obtained during the acute infection. The proliferative responses to PHA were restored by the addition of gamma-irradiated autologous convalescent or allogeneic PBMC. Cell contact with the irradiated PBMC was necessary to restore proliferation. Non-T cells from the acute PBMC of dengue patients did not support proliferation of T cells from control donors in response to PHA, but T cells from the PBMC of patients with acute dengue proliferated if accessory cells from a control donor were present. Addition of anti-CD28 Abs restored anti-CD3-induced proliferation of the PBMC of some patients. The percentage of monocytes was reduced in the acute sample of PBMC of the dengue patients. Addition of IL-2 or IL-7, but not IL-4 or IL-12, also restored proliferation of acute PBMC stimulated with anti-CD3. The results demonstrate that both quantitative and qualitative defects in the accessory cell population during acute dengue illness result in a depression of in vitro T cell proliferation.
authors.affiliation: Center for Infectious Disease and Vaccine Research, University of Massachusetts Medical Center, Worcester 01655, USA.
authors.forename: A
authors.initials: A
authors.lastname: Mathew
authors.forename: I
authors.initials: I
authors.lastname: Kurane
authors.forename: S
authors.initials: S
authors.lastname: Green
authors.forename: D W
authors.initials: DW
authors.lastname: Vaughn
authors.forename: S
authors.initials: S
authors.lastname: Kalayanarooj
authors.forename: S
authors.initials: S
authors.lastname: Suntayakorn
authors.forename: F A
authors.initials: FA
authors.lastname: Ennis
authors.forename: A L
authors.initials: AL
authors.lastname: Rothman
mesh_terms: D000208:Acute Disease; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D000938:Antigen-Presenting Cells / Q000276:immunology; D000956:Antigens, Viral / Q000494:pharmacology; D018106:CD28 Antigens / Q000276:immunology; D002450:Cell Communication / Q000276:immunology / Q000528:radiation effects; D002648:Child; D003715:Dengue / Q000276:immunology*; D003716:Dengue Virus / Q000276:immunology; D005720:Gamma Rays; D006801:Humans; D007108:Immune Tolerance / Q000276:immunology* / Q000528:radiation effects; D018664:Interleukin-12 / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D015847:Interleukin-4 / Q000494:pharmacology; D015851:Interleukin-7 / Q000494:pharmacology; D007958:Leukocyte Count; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000528:radiation effects; D008213:Lymphocyte Activation / Q000276:immunology* / Q000528:radiation effects; D018655:Lymphocyte Count; D009000:Monocytes / Q000276:immunology; D010835:Phytohemagglutinins / Q000494:pharmacology; D011994:Recombinant Proteins / Q000494:pharmacology; D019595:Severe Dengue / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D013745:Tetanus Toxoid / Q000494:pharmacology
chemical_list: D000911:Antibodies, Monoclonal; D000956:Antigens, Viral; D018106:CD28 Antigens; D007376:Interleukin-2; D015851:Interleukin-7; D010835:Phytohemagglutinins; D011994:Recombinant Proteins; D013745:Tetanus Toxoid; D018664:Interleukin-12; D015847:Interleukin-4