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Journal of Virology, January 2000, p. 552-555, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Immune Complexes Containing Human Immunodeficiency
Virus Type 1 Primary Isolates Bind to Lymphoid Tissue B Lymphocytes and
Are Infectious for T Lymphocytes
Jocelyn J.
Jakubik,
Mohammed
Saifuddin,
Daniel M.
Takefman, and
Gregory T.
Spear*
Department of Immunology/Microbiology, Rush
University, Chicago, Illinois 60612
Received 23 June 1999/Accepted 22 September 1999
 |
ABSTRACT |
This study investigated the interaction of tonsil B lymphocytes
with immune complexes containing human immunodeficiency virus (HIV IC)
primary isolates and the infectivity of the B cell-bound HIV IC.
Treatment of virus with a source of antibody and complement increased
HIV IC binding to B cells by 5.6-fold. Most of the HIV IC that bound to
B cells were not internalized but remained on the cell surface and were
gradually released over 72 h. Cell-bound HIV IC were highly
infectious for T cells while virus released by cultured B cells was
only slightly infectious. Removal of HIV IC from the B-cell surface by
protease treatment reduced the infection of T cells to near-background
levels, indicating that infectious virus remained on the B-cell
surface. These studies show that B lymphocytes can carry and transfer
infectious HIV IC to T cells and thus suggest a novel mode of infection
of T cells in lymphoid tissue that could be important for pathogenesis
during HIV infection.
| |
TEXT |
During infection with human
immunodeficiency virus type 1 (HIV-1), plasma virus can reach levels as
high as millions of virus particles/milliliter (12, 16), and
a portion of this plasma virus is in the form of immune complexes
(14, 15, 19, 20). High levels of HIV are also found in
lymphoid tissues, including lymph nodes (reviewed in references
3 and 8), and the total amount of
virus found in this compartment within infected individuals has been
estimated at 5 × 1010 virions (9). A large
portion of this virus is associated with the surfaces of follicular
dendritic cells (FDC) within follicles, and it is thought that FDC trap
these HIV particles on their surfaces as immune complexes along the
network of dendrites which express complement receptor 1 (CR1), CR2,
CR3, and Fc receptors (7, 13).
Several studies suggest that FDC may play a role in the pathogenesis of
HIV infection by transferring infectious immune complexes containing
HIV (HIV IC) to T cells during cell-cell contact in follicles although
it appears that FDC themselves do not become infected (5, 10, 17,
18). One study provided evidence that FDC may be particularly
efficient in transferring HIV IC to T cells by showing that virus
complexed with neutralizing antibody was not infectious when incubated
with T cells but that the virus-antibody complexes were infectious for
T cells when bound to FDC (10).
B lymphocytes within lymphoid tissues play critical roles in immune
responses and are densely concentrated in and around the follicles of
lymphoid tissue, where they interact with T cells and FDC to receive
signals for clonal expansion, affinity maturation, and class switching
(reviewed in reference 1). Since B cells in lymphoid
tissues express CR1 and CR2 (CD35 and CD21, respectively) and the
FcRIIB1 receptor (CD32) (4), which allow them to bind immune
complexes, we reasoned that B cells might also be able to trap HIV IC
and transfer them to T cells. Thus, in this study, we investigated
several important features of the B-cell-HIV IC interaction, including
(i) whether B cells from lymphoid tissues can bind HIV IC, (ii) the
localization of the HIV IC after binding to B cells, and (iii) if the
bound HIV IC are infectious for T cells. Cell-cell interactions such as
these, which could result in the transfer of infectious HIV to T cells
in vivo, are likely to contribute to HIV pathogenesis.
Binding of primary isolate HIV IC to tonsillar B lymphocytes.
We first assessed the binding of HIV IC made with primary isolates (PI)
of HIV-1 from three different patients to B cells isolated from
tonsils. Autologous patient serum (taken from the same donor and at the
same time as the virus isolate) was heat inactivated and used as an
antibody source for each isolate, and the binding of HIV IC to B cells
was assessed for virus treated with complement only, heat-inactivated
complement (HIC) only, antibody plus complement, antibody plus HIC, and
HIV incubated without antibody or complement. Previous studies have not
investigated the interaction of B cells or FDC with HIV IC containing PI.
All three control-treated virus isolates bound at relatively low
levels, with 7 to 31 pg of p24 bound to 2 × 106 B
cells (Fig. 1). Treatment with HIC or
autologous serum plus HIC did not significantly increase virus binding
(P > 0.05, t test). Treatment of virus with complement
alone increased binding by an average of 2.4-fold (4.2-, 1.3-, and
1.9-fold for isolates 1, 2, and 3, respectively) (P > 0.05) while treatment with autologous serum plus complement
significantly increased the amount of virus binding to B cells by an
average of 5.6-fold (7-fold for isolate 1 and about fivefold for both
isolates 2 and 3), compared to the level of binding of control-treated
HIV (P < 0.05). The immunoglobulin G (IgG) in sera
appeared to be responsible for the increased binding of HIV to B cells
since treatment of PI 1 with complement plus protein G-purified IgG
from serum sample 1 at 1 and 0.25 mg/ml increased p24 binding by 7- and
4.9-fold, respectively, over complement-alone treatment while IgG from
an HIV-seronegative donor did not increase HIV binding (not shown).
Taken together, these data indicate that treatment of virus with both
complement plus the antibody source was necessary for the highest level
of HIV IC binding since heat inactivation of complement reduced bound
virus to control levels. These data also demonstrate that treatment
with complement alone induced some virus binding to B lymphocytes.
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FIG. 1.
Binding of HIV IC to tonsil B lymphocytes. Tonsil B
cells (2 × 106) were incubated for 2 h at 4°C
with HIV IC, which were prepared by incubating HIV PI (6,000 pg of p24)
from three different subjects (PI 1 [A], PI 2 [B], and PI 3 [C])
with heat-inactivated (56°C for 45 min) autologous patient plasma
(final dilution, 1:30) as a source of antibody (Ab) and with normal
human serum from a seronegative AB+ donor as a source of
complement (C) or HIC (final dilution, 1:10) for 50 min at 37°C
(final incubation volume of 200 µl). Cells were washed and then lysed
with 0.5% Triton X-100, and the amount of cell-bound virus was
determined by a p24 ELISA (AIDS Vaccine Program, National Institutes of
Health, Frederick, Md.). Each bar represents the mean ± the
standard error of the mean of results from three experiments. HIV-1 PI
were obtained by coculturing 2 × 106 PBMC from
HIV-infected donors at a 1:1 ratio with PBMC from an uninfected donor
that were prestimulated for 3 days with 3 µg of PHA (Sigma Chemical
Co., St. Louis, Mo.) per ml and 25 U of interleukin-2 (Boehringer
Mannheim, Indianapolis, Ind.) per ml (21). All three PI
donors were asymptomatic. Tonsil mononuclear cells were separated by
the teasing of tonsil tissue, followed by filtration through a
70-µm-pore-size nylon Spectra/Mesh filter (Spectrum Medical Industry,
Inc., Houston, Tex.) before being washed with RPMI 1640 (Whittaker
Bioproducts, Walkersville, Md.) culture medium containing 1%
L-glutamine, 25 mm HEPES, 10% heat-inactivated fetal
bovine serum (Whittaker Bioproducts), and gentamicin (Sigma). B cells
were isolated by negative selection with a mixture of anti-CD8 and
anti-CD4 magnetic Dynabeads (M-450) (Dynal, Oslo, Norway). The
resultant B-cell-enriched preparations were >95% CD19+.
|
|
Since more than 95% of tonsil B cells express CR2 and since this
receptor is important for binding immune complexes to B cells,
CR2 was
studied for its role in binding HIV IC produced by the
incubation of
virus with autologous serum and complement. The
PI and serum from
patient 1 was used to make HIV IC in all further
experiments since this
combination yielded the greatest increase
in binding to B cells in the
presence of complement (Fig.
1).
Preincubation of B cells with anti-CR2
monoclonal antibody OKB7
blocked 76% of the binding of HIV IC to B
cells (Fig.
2). However,
anti-LFA-1
antibody, which also binds to B cells, did not substantially
block HIV
IC binding (Fig.
2). Thus, although antibodies directed
to LFA-1 have
been shown to reduce HIV infectivity at the initial
virus-cell
interaction as well as at later stages of infection
(
11),
anti-LFA-1 antibodies did not significantly inhibit the
binding of HIV
IC to tonsil B lymphocytes.
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FIG. 2.
Inhibition of binding of HIV IC to tonsil B lymphocytes
by anti-CR2 antibody. Tonsil B cells were preincubated without or with
antibody to CR2 (OKB7; Ortho Diagnostic Systems, Raritan, N.J.) or
LFA-1 (anti-CD11a, clone 38; ID Labs, London, Ontario, Canada) (each at
1.0 µg/ml) for 1 h at room temperature prior to addition of HIV
IC. Cells were then incubated for 2 h at 4°C with HIV IC, which
were prepared by the incubation of PI 1 with autologous serum and
complement (see details in the Fig. 1 legend). Cells were washed and
lysed with 0.5% Triton X-100, and the amount of cell-bound virus was
determined by a p24 ELISA. Means ± standard errors of results
from triplicate samples are shown. This experiment is representative of
three experiments.
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|
Localization of HIV IC after binding to tonsil B lymphocytes.
The next studies determined the localization of B-cell-bound HIV IC in
cultures. Tonsil B cells were incubated with HIV IC made with PI 1 plus
autologous serum and complement. Cells were then washed and cultured
for 72 h. The amount of HIV IC associated with B cells decreased
from 189 pg of p24 (100%) bound at time 0 to approximately 124 pg
(66%) at 15 h, 113 pg (60%) at 24 h, 47 pg (25%) at
48 h, and 38 pg (20%) at 72 h (Fig.
3). Surprisingly, most of the HIV IC
appeared to remain on the surfaces of the B cells since the treatment
of cells with proteinase K at each time point substantially reduced
detection of the virus (Fig. 3), while the protease treatment did not
decrease the cell number or viability (data not shown). However, at all
time points there was a small amount of protease-resistant p24
associated with B cells, suggesting some internalization (Fig. 3).
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FIG. 3.
Localization of HIV IC in B-cell cultures. Tonsil B
cells were incubated for 2 h at 4°C with HIV IC, which were
prepared by preincubation of PI 1 with matched autologous serum and
complement (see details in Fig. 1 legend). Cells were washed and
cultured for 72 h in complete medium in 24-well plates (2 × 106 cells/ml). At 0, 15, 24, 48, and 72 h, cells were
washed and lysed with 0.5% Triton X-100 and the amount of
cell-associated virus was determined by p24 ELISA. The total amount of
virus released was also measured in the supernatant after treatment
with 0.5% Triton X-100. The amount of intact released virus in a
supernatant was calculated by subtracting the free p24 measured in the
absence of detergent from the total amount of released p24. Some
aliquots of B cells were treated with proteinase K (1.0 µg/ml; Sigma)
in serum-free medium for 10 min before the cells were washed and lysed
with 0.5% Triton X-100 to assess the amount of protease-resistant p24
associated with B cells. The means of results from three
experiments ± the standard errors of the means are shown.
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|
At 15 h, 87 pg (46%) of the p24 had been released into the
culture medium, and this amount increased to 111 pg (59%) at 48
h. Most of the released p24 appeared to be retained within an
intact
virus membrane, since the majority of this released p24
was
undetectable in the absence of detergent. Thus, at 15, 24,
48, and
72 h there was 51, 59, 79, and 51 pg of p24 antigen, respectively,
released from B lymphocytes that appeared to be intact
virus.
Infection of PBMC by B-cell-bound HIV IC.
The above studies
indicated that HIV IC could remain on the surfaces of tonsil B
lymphocytes for up to 3 days and that a portion of the released p24 may
have intact membranes. We thus investigated whether the released or
cell-bound virus remained infectious for phytohemagglutinin
(PHA)-stimulated peripheral blood mononuclear cells (PBMC). HIV IC were
prepared by the treatment of PI 1 with autologous serum and complement
and incubation with B cells, and the B cells were cultured as described
in the Fig. 2 legend. The B cells and B-cell culture supernatants were
harvested at 0, 24, 48, and 72 h and cultured with PHA-stimulated
PBMC for 12 days. After 12 days, the PBMC cultures were analyzed for
virus replication by a p24 enzyme-linked immunosorbent assay (ELISA).
The p24 levels in the PBMC cultures which contained the B-cell
supernatants ranged from 346 ± 69 to 979 ± 223 (mean ± standard
error of the mean) pg/ml, indicating that some infectious
virus
had been released from the tonsil B lymphocytes over the course
of 72 h (Table
1). In contrast, the
p24 levels from PBMC cultures
which contained the tonsil B cells ranged
from 16,787 ± 1,487
to 20,106 ± 1,576 pg/ml, indicating
that B-cell-bound HIV IC were
substantially more infectious for T cells
than was released virus.
The p24 levels in PBMC cultures which
contained proteinase K-treated
B cells ranged from 106 ± 1 to
537 ± 5 pg/ml, indicating that
most of the infectious virus
remained on the surfaces of B cells.
Less than 80 pg of p24 was
detected when tonsil B cells with bound
HIV IC were cultured for 12 days in the absence of PHA-stimulated
PBMC, indicating that the high
infection levels which were detected
in cocultures were due to
infection of the PHA-stimulated PBMC
and not B lymphocytes. Thus, these
data suggest that HIV IC bound
to B cells can remain infectious for T
cells for up to 72 h following
the initial virus-B-cell
interaction. These data also show that
released HIV IC were still
slightly infectious, but that HIV IC
which remained bound to the B-cell
surface were much more infectious
for T cells.
This report shows that B cells from lymphoid tissue can bind HIV IC
that contain PI of HIV and, during a subsequent cell-cell
interaction,
transfer the infectious virus to T cells. This suggests
a novel mode of
infection of T cells that is analogous to the
mode of infection
proposed by others, in which FDC-bound virus
can infect T cells
(
5,
10). While in situ studies of lymph
nodes from
HIV-infected persons show that most HIV IC appear to
be associated with
FDC (
3,
8), T cells may have more opportunities
to interact
with B cells than with FDC in lymphoid tissue, and
thus infectious HIV
IC carried by B cells could also be an important
means of T-cell
infection in vivo. For example, a recent study
showed that during
immune responses in lymph nodes, B-cell-T-cell
interactions occurred
at the border of the follicles and few T
cells were observed inside
follicles, where FDC are located (
6).
This is also the first
study to investigate how PI behave in these
types of studies. Thus,
previous studies of HIV IC interaction
with cells used
T-cell-line-adapted strains of virus for interaction
with FDC (
5,
10) and other studies show that T-cell-line-adapted
virus
interacts with antibodies very differently than PI (
2).
The observation that a significant and infectious fraction of HIV IC
could remain on the surfaces of B cells for as long as
72 h is
striking and potentially important for the infection of
T cells in
lymph nodes. Little information regarding the fate
of immune complexes
that bind to B cells is available, although
Thornton et al.
(
22) observed that while immune complexes containing
keyhole
limpet hemocyanin (KLH), anti-KLH, and complement bound
to all B cells,
only KLH-specific B cells processed the KLH into
peptides, suggesting
that HIV IC would bind to, but not be internalized
by, most B cells.
Unexpectedly, the infection of PHA-stimulated
PBMC by B-cell-bound HIV
IC increased over a 72-h period (Table
1) even though the amount of p24
bound to B cells decreased over
this period (Fig.
3). The explanation
for this apparent increased
infectivity is not known, although we
speculate that changes in
the B-cell activation state over time could
affect the efficiency
of interaction between B cells and T cells and
the resultant infection
rate of T
cells.
Another interesting observation was that although about 30 to 40% of
the virus that was initially bound to the B cells was
released into the
medium during the first 24 to 48 h of culture,
this virus was
essentially noninfectious. While it appeared that
the majority of the
released virus had an intact membrane, since
detergent was required for
the detection of p24, the lack of infection
suggested that some
degradation of the virus or virus proteins
took place while bound to B
cells. In conclusion, these studies
show that B cells can bind and
transfer infectious HIV IC to T
cells and thus suggest a novel means of
infection of T cells in
vivo.
| |
ACKNOWLEDGMENTS |
This work was supported by National Institutes of Health grant
AI-31812.
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Department of
Immunology/Microbiology, Rush University, 1653 W. Congress Pkwy.,
Chicago, IL 60612. Phone: (312) 942-2083. Fax: (312) 942-2808. E-mail: gspear{at}rush.edu
| |
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Journal of Virology, January 2000, p. 552-555, Vol. 74, No. 1
0022-538X/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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