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Expansion of restricted cellular immune responses to HIV-1 envelope by vaccination: IL-7 and IL-12 differentially augment cellular proliferative responses to HIV-1

Kim, JH and Loveland, JE and Sitz, KV and Ratto Kim, S and Mclinden, RJ and Tencer, K and Davis, K and Burke, DS and Boswell, RN and Redfield, RR and Birx, DL (1997) Expansion of restricted cellular immune responses to HIV-1 envelope by vaccination: IL-7 and IL-12 differentially augment cellular proliferative responses to HIV-1. Clinical and Experimental Immunology, 108 (2). 243 - 250. ISSN 0009-9104

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Abstract

The failure of immune effector mechanisms to control HIV-1 infection has important consequences for the human host. In a randomized cohort of HIV- infected patients, there was striking in vitro restriction of the proliferative response to HIV-1 envelope protein (Env), gp160; only 34% of patients recognized Env. Therapeutic vacci nation with recombinant gp160 or gp120 (rgp160, rgp120) reversed the restriction in vitro, with Env recognition rising to 81%. Peripheral blood mononuclear cells (PBMC) from HIV-infected vaccine recipients, placebo recipients, and seronegative volunteers were cultured with exogenous IL-7 or IL-12 and either tetanus toxoid (TT) or gp160. IL-7 significantly augmented proliferative responses to TT and gp160, whereas IL-12 only affected proliferation to gp160. IL-7, but not IL-12, increased the number of HIV-infected placebo recipients who recognized rgp160. IL-12 had its greatest effect in the induction of rgp160- specific responses from seronegative individuals. The data suggest that these two cytokines have differential activity in the relief of restricted cellular immunity to Env; the predominant effect of IL-7 is in individuals who have been primed by exposure to antigen, while the effect of IL-12 is most evident in seronegative, unprimed individuals. Modification of restricted proliferative responses to Env by vaccination or cytokines in vitro suggests that strategies incorporating IL-7 or IL-12 as adjuvants may selectively boost cellular reactivity to HIV-1.


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Kim, JH
Loveland, JE
Sitz, KV
Ratto Kim, S
Mclinden, RJ
Tencer, K
Davis, K
Burke, DSdonburke@pitt.eduDONBURKE
Boswell, RN
Redfield, RR
Birx, DL
Centers: Other Centers, Institutes, or Units > Center for Vaccine Research
Date: 9 June 1997
Date Type: Publication
Journal or Publication Title: Clinical and Experimental Immunology
Volume: 108
Number: 2
Page Range: 243 - 250
Schools and Programs: Graduate School of Public Health > Epidemiology
Refereed: Yes
ISSN: 0009-9104
Date Deposited: 07 May 2015 19:28
Last Modified: 03 Feb 2018 14:55
URI: http://d-scholarship.pitt.edu/id/eprint/24402

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