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IMMUNOBIOLOGY
From the Department of Cell Biology, Faculty of
Biology, Complutense University, Madrid, Spain.
Despite the information dealing with the differential phenotype and
function of the main mouse dendritic cell (DC) subpopulations, namely,
CD8 Dendritic cells (DCs) play a central role in the
immune system due to their main function as initiators and regulators
of antigen-specific antiviral T-cell responses and in the pathogenesis of a variety of viruses, such as human immunodeficiency virus (HIV),
cytomegalovirus, measles virus, herpes virus, influenza virus, and
respiratory syncytial virus.1 However, little is known
about the subpopulations of DCs involved in antiviral responses, the
kinetics of the variations of DC subpopulations, and, importantly, the
mechanisms of recruitment of DCs to the lymph nodes (LNs) during
inflammatory responses driven by viral infections. On the other hand,
despite the available information dealing with the phenotype and
function of the 2 main mouse DC subsets, namely, CD8 Over the last years CD8 Experimental infection with MMTV(SW)
LN DC isolation
A DC-enriched cell fraction was then obtained after depletion of T
cells, B cells, and granulocytes by treating the 1.061-density fraction
for 50 minutes at 4°C with a monoclonal antibody (mAb) mixture
including anti-CD3 (clone KT3-1.1), anti-B220 (clone RA3-6B2), and
antigranulocyte antigen Gr1 (clone RB6-8C5). The unwanted cells were
then removed magnetically after incubation for 30 minutes at 4°C with
anti-rat Ig-coated magnetic beads (Dynabeads, Dynal, Oslo, Norway) at
a 7:1 bead-cell ratio. Analysis of CD11c expression revealed that
DC-enriched cell fractions, used for flow cytometric analysis, were
composed of 50% to 80% DCs, as shown in Figure 1A.
For PCR experiments with day 2 PO-LNs or day 6 MS-LNs, DCs were purified by magnetic cell sorting (MACS) with MACS separation columns (Miltenyi Biotec, Bergisch, Germany) after incubation of the DC-enriched cell fraction with biotinylated anti-CD11c mAbs, followed by streptavidin-conjugated MACS microbeads (Miltenyi Biotec). After reanalysis, the DC fraction had a purity of more than 98% (data not shown). For PCR experiments with day 6 PO-LNs, CD8+ DCs were
purified with MACS separation columns after incubation of the
DC-enriched cell fraction with biotinylated anti-CD8 Blood DC isolation Heparinized blood was incubated for 30 minutes at 4°C in an ammonium chloride potassium lysis buffer to remove red blood cells (RBCs), washed twice in PBS-EDTA-FCS, and filtered through a stainless-steel sieve. T cells, B cells, and granulocytes were depleted with magnetic beads as described above; FACS analysis revealed that blood DC-enriched cell fractions, used for phenotypic analysis, were composed of more than 50% CD11c+ cells, as shown in Figure 5A.Blockade of cell migration from the blood to the PO-LNs Blocking of MMTV(SW)-induced blood cell migration via HEVs was achieved by intravenous injection of purified anti-CD62L (L-selectin) antibodies (clone Mel-14), into mice that were injected 36 hours before with MMTV(SW). These mice were analyzed 36 hours after anti-CD62L treatment, that is, at day 3 after MMTV(SW) injection.LC migration assays Control or MMTV(SW)-injected BALB/c mice received 10µL 1% fluorescein isothiocyanate (FITC; Sigma, St Louis, MO) dissolved in 1:1 acetone-dibutyl phthalate on the hind footpad, and were analyzed after 3 days for the presence of FITC+ DCs in the draining PO-LNs.Flow cytometry Analysis of PO-LN DCs was performed after triple staining with FITC-conjugated anti-CD11c (clone N418), phycoerythrin (PE)-conjugated anti-CD8 (clone CT-CD8a, Caltag, San Francisco, CA), and
biotin-conjugated anti-CD11b (Mac-1; clone M1/70), anti-DEC-205 (clone
NLDC-145), anti-CD4 (clone GK1.5) or antileukocyte function-associated
antigen (LFA)-1 (clone FD441.8) followed by
streptavidin-tricolor (Caltag). Blood DCs were analyzed after triple
staining with FITC-conjugated anti-CD11c, PE-conjugated antimajor
histocompatibility complex (MHC) class II (clone M5/114.15.2,
Pharmingen, San Diego, CA), and biotin-conjugated anti-CD11b,
anti-DEC-205, anti-CD8 (clone 53-6.72), anti-CD4, anti-CD86 (B7-2;
clone GL1, Pharmingen), anti-CD40 (clone FGK45), anti-F4/80 (clone
C1.A3.1), or anti-CD62L (L-selectin; clone Mel-14) followed by
streptavidin-tricolor. Detection of FITC+ cells was
achieved after double staining with PE-conjugated anti-CD11c (Pharmingen) and tricolor-conjugated anti-CD8 (Caltag). Analyses were performed on a FACSort instrument (Becton Dickinson, Mountain View, CA).
Electron microscopy The PO-LNs were fixed with 1% glutaraldehyde and 1% paraformaldehyde in 0.1 M pH 7.6 Sørensen phosphate buffer for 2 hours at 4°C, postfixed with 1% OsO4 in the same buffer for 1 hour at 4°C, dehydrated in graded acetone solutions, and embedded in Embed-812 (Electron Microscopy Sciences, Washington, PA). Semithin sections (1 µm) were stained with toluidine blue and photographed in a Zeiss Axioskop microscope (Zeiss, Oberkochen, Germany), and ultrathin sections (70-80 nm) were counterstained with uranyl acetate and lead citrate and examined with a Jeol 1010 electron microscope (Jeol, Tokyo, Japan).PCR analysis of DC infection by MMTV(SW) DNA isolated from highly purified DCs, obtained from PO-LNs or MS-LNs at the indicated times, was amplified using the MMTV(SW) open reading frame (orf)-specific primers 5'-TGG CAA CCA GGG ACT TAT AGG and 3'-GCG ACC CCC ATG AGT ATA TTT, yielding a 316-kb PCR product. PCR was performed on a GeneAmp PCR System 9700, using 2,5 U AmpliTaq Gold polymerase per PCR reaction (Perkin-Elmer, Foster City, CA). PCR conditions were 10 minutes at 95°C, followed by 40 cycles of 30 seconds at 94°C, 30 seconds at 62°C, and 30 seconds at 72°C, and finally 7 minutes at 72°C. PCR products were analyzed on agarose gels stained with ethidium bromide and photographed with a Nikon Coolpix 950 digital camera (Nikon, Tokyo, Japan).
Changes in the PO-LN DC subsets after MMTV(SW) injection During the first week after injection of MMTV(SW) in the rear footpad of BALB/c mice, important changes occurred in the relative proportions corresponding to the different DC subsets present in the PO-LNs, as illustrated in Figure 1A. As previously described for pooled peripheral LNs,4 3 DC subsets can be defined in the PO-LNs of control mice on the basis of the CD11c versus CD8 expression, namely CD8 ,
CD8int, and CD8+ DCs, which represented around
15%, 75%, and 10% of total PO-LN DCs, respectively. Injection of
MMTV(SW) determined a strong increase in the percentage of both
CD8 and CD8+ subsets, constituting around
70% and 25%, respectively, at day 6. This was paralleled by a
dramatic reduction in the percentage of CD8int DCs that
constituted around 10% of total DCs at this time. The analysis of the
absolute DC number within each PO-LN subset (Figure 2) revealed that the variations in the
relative proportion of these DC subsets induced by MMTV(SW) injection
were the result of a considerable augmentation of the CD8
and CD8+ DC number during the first week after injection,
whereas the absolute number of CD8int DCs did not undergo
significant variations. By day 3, approximately a 20- and 7-fold
increase in CD8 and CD8+ DC number was
induced by virus injection. By day 6, the cell number increase was 45- and 30-fold for CD8 and CD8+ DCs,
respectively, corresponding to approximately an 18-fold increase in the
total DC number at this time. Interestingly, the increase in the
absolute number of B cells and T cells was approximately 14- and
4-fold, respectively, at day 3, and 25- and 12-fold at day 6 (data not
shown). Therefore, the increase in the number of DCs, specially of the
CD8 subset, induced by MMTV(SW) was significantly higher
than the increase of B or T cells, despite the fact that both
lymphocyte subsets underwent a strong proliferative response during
MMTV(SW) infection.7,9 This increase in DC number was
concomitant with the presence of high numbers of DCs in the outer
cortex of the PO-LNs, in close association with HEVs, as revealed by
light and electron microscopy (Figure 3).
DCs were almost undetectable in control PO-LN sections (not
shown).
By day 10 an important reduction in all the DC subsets was detected,
which corresponded to the extinction of the immune response against
MMTV(SW), occurring during the second week after virus injection.7 Interestingly, the comparison of the increase
in the absolute number of CD8 The study of the kinetics of the different PO-LN DC subsets after
MMTV(SW) injection described above was performed together with an
analysis of the expression of a number of DC markers that have been
proven to be decisive in the definition of mouse DC subpopulations,
such as CD11b (Mac-1), DEC-205, CD4, and LFA-1.4,10,11 No
significant phenotypic differences were noticed after virus challenge
regarding these markers, except for the expression of CD4 by the
CD8 Blockade of MMTV(SW)-induced increase of PO-LN DC number by anti-CD62L treatment Because DCs are considered to be nondividing cells once they have reached peripheral lymphoid organs, the increase in DC number after MMTV(SW) injection could reflect a massive entry of DCs to the PO-LNs. The fact that this increase affected CD8 and
CD8+ DCs, but not CD8int DCs, which in the case
of peripheral LN CD8int DCs have been demonstrated to
derive from epidermal LCs,4 indicated that MMTV(SW)
injection most likely caused the recruitment of DCs from the
bloodstream via HEVs. To test this hypothesis, 36 hours after virus
challenge, mice were injected with purified anti-CD62L antibodies
(clone Mel-14), which block leukocyte migration through
HEVs.12 These mice were analyzed 36 hours later, that is,
at day 3 after MMTV(SW) injection. As illustrated in Figure 4, anti-CD62L treatment caused an almost
complete inhibition of the increase in CD8 and
CD8+ DC number induced by MMTV(SW), whereas the
CD8int DC subset remained unaffected. This result suggested
that a massive entry of blood DCs via HEVs, responsible for the rise in
PO-LN DC number, was induced by MMTV(SW), and revealed that this
occurred by a CD62L-dependent mechanism.
To further define MMTV(SW)-induced DC recruitment to the LNs, an
analysis of blood DC phenotype was performed, because to our knowledge
mouse blood DCs had not been previously characterized. For this
purpose, a DC-enriched cell suspension was obtained from BALB/c mice,
after treatment of heparinized blood with lysis buffer, followed by
magnetic bead depletion, as described in "Materials and methods."
Blood DCs, defined as CD11c+ cells, displayed a pattern of
cell surface marker expression resembling that previously reported for
spleen and LN CD8
In conclusion, because MMTV(SW) induced the entry to the LN of blood
DCs, negative for CD8, leading to an increase not only of
CD8 Inhibition of LC migration to the draining LNs during MMTV(SW) infection With regard to CD8int DCs, as mentioned above, this DC subset did not undergo significant variations after MMTV(SW) injection and, on the other hand, anti-CD62L treatment did not determine significant variations in the absolute cell number within this population. These data suggest that PO-LN CD8int DCs do not derive from blood-borne DCs, but rather that they gain access to the PO-LNs via afferent lymphatics, in agreement with previous data from our group4 demonstrating that CD8int DCs located in auricular LNs derive from ear epidermal LCs.To test whether this was the case, the rear footpad of BALB/c mice was
labeled with a FITC solution, and the PO-LNs analyzed after 3 days. As
expected, FITC+ DCs were found mainly within the
CD8int DC subset (Figure 6A),
where they represented up to 45% of the cells (approximately 900 CD8int FITC+ DCs per PO-LN in the experiment
illustrated in Figure 6), confirming that these cells derived from LCs
that had migrated to the PO-LN. The CD8
PCR analysis of DC infection by MMTV(SW) The data presented in this report revealed that during the infection by MMTV(SW), the PO-LN DCs underwent profound variations involving a massive recruitment of DCs via HEVs. On the other hand, in a recent report, the involvement of DCs in early phases of MMTV(SW) infection has been suggested,13 although no direct evidence of DC infection by MMTV has been reported yet. On the basis of these results we have investigated whether PO-LN DCs become infected after MMTV(SW) injection. For this purpose, highly purified DCs were analyzed for the presence of MMTV(SW) DNA after integration in the target cell genome by PCR, using primers specific for MMTV(SW). To address whether DCs were infected during the early phases of the process of MMTV(SW) infection, when the first infected B cells can be detected,14 PO-LN DCs were purified from mice injected 48 hours before with the virus. To test whether CD8 or
CD8+ DCs (or both) were infected, these DC subsets were
purified from PO-LNs, 6 days after virus injection. Our results, shown
in Figure 7, demonstrate that MMTV(SW)
DNA can be detected in DCs from day 2 PO-LNs, and in both
CD8 and CD8+ DCs isolated from day 6 PO-LNs,
but not in DCs isolated from day 6 MS-LNs, used as control DCs. These
data support that DCs could participate in the first phases of MMTV(SW)
infection, as previously proposed.13 Finally, the fact
that both CD8 and CD8+ DCs were infected at
later phases of the infection process, suggest that DCs could be
involved in viral transmission to the mammary gland, as described for
extrafollicular plasmablasts.7
The immune response against MMTV involves a strong B-cell proliferative response that determines the amplification of the few initially infected B cells, required for an efficient infection process leading ultimately to the transmission of MMTV to the mammary gland and to the progeny.15 Previous studies using an experimental MMTV infection model, in which the immune response against MMTV can be analyzed in the PO-LNs after virus injection into the hind footpad of BALB/c mice, revealed that MMTV determined an inflammatory response in the PO-LN causing the influx of B and T cells from the bloodstream via HEVs.7,9 In the present study, we have analyzed the behavior of the PO-LN DC
subsets during the infection by MMTV(SW). Injection of MMTV(SW) induced
a massive increase in the number of DCs in the PO-LN caused by the
entry of blood-borne DCs. Although it has been previously reported that
Rauscher leukemia virus infection was accompanied by an increase in
peripheral LN DCs,16 our data provide the first evidence
of a massive DC recruitment from the blood to the LNs via HEVs driven
by an inflammation/viral infection process. In addition, our blocking
experiments using anti-CD62L mAbs demonstrated that DC recruitment to
the LNs occurred by a CD62L-dependent mechanism, as previously shown
for lymphocytes and granulocytes,12 but not for DCs.
Interestingly, whereas DCs located extravascularly in lymphoid organs
such as the spleen, Peyer patches, and thymus do not express the homing
receptor CD62L,4 which has been demonstrated to be
involved in leukocyte migration to peripheral LNs via
HEVs,12 around 50% of blood CD11c+ DCs
expressed this molecule, which, as shown here, participates in DC
recruitment to the LNs. Concerning CD4 expression, blood DCs are
negative for this marker, whereas about 70% of splenic DCs are
CD4+.2 However, although control PO-LN
CD8 With regard to the different PO-LN DC subsets, in control mice the
majority of DCs correspond to the LN-related subset of CD8int DCs,4,17 which has been claimed to
derive from epidermal LCs in the case of peripheral LNs
CD8int DCs, and from intestinal lamina propria DCs for
MS-LN CD8int DCs (F.A., manuscript in preparation). During
the infection process by MMTV(SW) a strong increase in the absolute
number of CD8 Taken together these data support the hypothesis that DC recruitment
from the blood determined an augmentation of the CD8 The concept that the generation of CD8+ DCs is the result
of a CD8 Finally, on the basis of a previous report13 claiming for
an essential role of DCs in the early phases of infection by MMTV(SW), we investigated whether DCs were infected by MMTV. Our results revealed
that DCs were infected by MMTV(SW) in the 48 hours after virus
injection, providing the first evidence of DC infection by MMTV. With
regard to the participation of DCs in viral infections, it has been
demonstrated that DCs play an essential role in the induction of the
antiviral immune response against HIV, by acting as initiators of the
activation of virus-specific T cells and more importantly, in HIV
transport and dissemination.27 In addition, DCs have been
claimed to be involved in the pathogenesis/response to a variety of
viruses, such as cytomegalovirus, measles virus, herpes virus,
influenza virus, and respiratory syncytial virus.1 In this
sense, the demonstration that PO-LN DCs are infected in the early
phases of the infection by MMTV(SW) could be related with their
presumed role of induction of the immune response against this virus,
because DCs have been demonstrated to be capable of presenting
efficiently MMTV(SW) superantigens to specific T
cells.28,29 Moreover, the fact that both CD8 In conclusion, our data derived from the study of DCs during the
infection by MMTV(SW) provide the first evidence of DC recruitment from
the blood via HEVs by a CD62L-dependent mechanism, as the result of a
viral infection-induced inflammatory response. In addition they
strongly support a functional correlation between CD8
The authors would like to thank Dr H. Acha-Orbea (Ludwig Institute for Cancer Research, Lausanne, Switzerland) for the MMTV-specific primers and Dr A. Rolink (Basel Institute for Immunology, Basel, Switzerland) for the anti-CD40 hybridoma FGK45.
Submitted August 23, 2001; accepted October 11, 2001.
Supported by the European Commission (grant no. QLRT-1999-00276), the Comunidad de Madrid of Spain (grant no. 08.1/0076/2000), and the Ministerio de Ciencia y Tecnología of Spain (grant no. BOS 2000-0558).
The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 U.S.C. section 1734.
Reprints: Carlos Ardavín, Dept of Cell Biology, Faculty of Biology, Complutense University, 28040 Madrid, Spain; e-mail: ardavin{at}bio.ucm.es.
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© 2002 by The American Society of Hematology.
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Top
Abstract
Introduction
) compared to control PO-LNs, in the CD8
, and secondary lymphoid organ chemokine.
J Exp Med.
2000;191:1381-1393