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.1997 Oct 28;94(22):12059-64.
doi: 10.1073/pnas.94.22.12059.

Targeting HIV proteins to the major histocompatibility complex class I processing pathway with a novel gp120-anthrax toxin fusion protein

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Targeting HIV proteins to the major histocompatibility complex class I processing pathway with a novel gp120-anthrax toxin fusion protein

T J Goletz et al. Proc Natl Acad Sci U S A..

Abstract

A challenge for subunit vaccines whose goal is to elicit CD8(+) cytotoxic T lymphocytes (CTLs) is to deliver the antigen to the cytosol of the living cell, where it can be processed for presentation by major histocompatibility complex (MHC) class I molecules. Several bacterial toxins have evolved to efficiently deliver catalytic protein moieties to the cytosol of eukaryotic cells. Anthrax lethal toxin consists of two distinct proteins that combine to form the active toxin. Protective antigen (PA) binds to cells and is instrumental in delivering lethal factor (LF) to the cell cytosol. To test whether the lethal factor protein could be exploited for delivery of exogenous proteins to the MHC class I processing pathway, we constructed a genetic fusion between the amino-terminal 254 aa of LF and the gp120 portion of the HIV-1 envelope protein. Cells treated with this fusion protein (LF254-gp120) in the presence of PA effectively processed gp120 and presented an epitope recognized by HIV-1 gp120 V3-specific CTL. In contrast, when cells were treated with the LF254-gp120 fusion protein and a mutant PA protein defective for translocation, the cells were not able to present the epitope and were not lysed by the specific CTL. The entry into the cytosol and dependence on the classical cytosolic MHC class I pathway were confirmed by showing that antigen presentation by PA + LF254-gp120 was blocked by the proteasome inhibitor lactacystin. These data demonstrate the ability of the LF amino-terminal fragment to deliver antigens to the MHC class I pathway and provide the basis for the development of novel T cell vaccines.

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Figures

Figure 1
Figure 1
Plasmid construct and fusion protein. (A) Plasmid NA125 construct for expression of LF254-gp120 fusion protein inE. coli. GST, 26-kDa glutathioneS-transferase domain from the parent vector pGEX-KG; LF1–254, coding sequences for residues 1–254 of mature LF; gp120, coding sequences for residues 1–511 of HXB2-env gene. (B) Expressed GST-LF254-gp120 protein. The carboxyl-terminal residue of the linker from pGEX-KG was changed from D to E, and four residues, TRLQ, were added between the LF254 and gp120 portions of the construct due to DNA manipulations. The V3 epitope, RGPGRAFVTI, recognized by CTL begins at residue 807 of the fusion protein.
Figure 2
Figure 2
Recognition of cells treated with gp120 anthrax toxin fusions by gp120-specific cytotoxic lymphocytes. The mouse mastocytoma cell line P815 was incubated with wild-type protective antigen (WPA) or mutant PACFD (MPA) and/or LF254-gp120 fusion proteins (50 ng/ml). P815 cells pulsed with 1.0 μM P18IIIB peptide served as a control. After 12 hr, the cells were washed and the treated P815 cells were labeled with51Cr. Labeled P815 cells were then mixed at different ratios with the CTL cell line 9.23.3, which recognizes the peptide sequence RGPGRAFVTI from gp120. Killing of the target cell population was determined by measuring release of51Cr into the medium (% lysis). Background lysis was determined with untreated,51Cr labeled, P815 cells. These data are the replicate of three experiments.
Figure 3
Figure 3
Inhibition of fusion protein processing by lactacystin. P815 cells were treated with 1 ng/ml of the GST-LF254-gp120 fusion protein alone and with PA (WPA) or mutant PA–D (DELPA) in the presence (B) or absence (A) of 10 μM lactacystin.51Cr-labeled target cells were mixed with α15–12 CTLs, and specific lysis was measured. Target cells were treated with the P18IIIB peptide as a positive control for cell lysis. These data are the representative of three experiments.
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