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IMMUNOBIOLOGY
From the Edward Jenner Institute for Vaccine Research,
Compton, Newbury, Berkshire, United Kingdom; Laboratory of Virology,
Istituto Superiore di Sanità, Rome, Italy; and INSERM
U255-Institut Curie, Paris, France.
Resting dendritic cells (DCs) are resident in most tissues and can
be activated by environmental stimuli to mature into potent antigen-presenting cells. One important stimulus for DC activation is
infection; DCs can be triggered through receptors that recognize microbial components directly or by contact with infection-induced cytokines. We show here that murine DCs undergo phenotypic maturation upon exposure to type I interferons (type I IFNs) in vivo or in vitro. Moreover, DCs either derived from bone marrow cells in vitro or
isolated from the spleens of normal animals express IFN- Dendritic cells (DCs) are recognized as the key
antigen-presenting cells (APCs) controlling the initiation of T
cell-dependent immune responses.1 DCs not only are the
most potent APCs for activation of resting T cells, but can also
regulate the type of response made, dictating the cytokines expressed
by responding T cells.2 Furthermore, DCs have the ability
to down-regulate T-cell activation and may play a role in the induction
of tolerance.3-5 The type of response elicited by
particular DCs is likely to reflect their developmental origin,
anatomical location, and state of activation.6
Immature (resting) DCs reside in most tissues and are efficient in
binding and internalizing antigens.1 However, these cells
are relatively poor at presenting antigen and inducing T-cell activation, owing at least in part to their low cell surface expression of costimulatory and adhesion molecules. In response to a variety of
stimuli (see below), DCs undergo a process that has been variably termed activation or maturation, during which they lose their capacity
for antigen uptake and acquire potent T-cell stimulatory ability. This
is associated with up-regulation of cell surface major
histocompatibility complex (MHC) class II, costimulatory molecules (eg,
CD80, CD86, CD40), and adhesion molecules (eg, CD54).1 DC
activation can be induced by signals that have been described as
indicative of "danger," such as heat shock proteins,7 mechanical manipulation,8 or exposure to necrotic
cells,8,9 as well as components of the extracellular
matrix,10 interaction with activated (CD40
ligand-expressing)T cells,11-14 and infection. DCs are particularly tuned to recognition of infection, as DC activation can be stimulated by exposure to whole pathogens (viruses or
bacteria15-17), components of micro-organisms (eg,
lipopolysaccharide [LPS], double-stranded RNA, CpG DNA, and
toxins15,18-21), and cytokines induced by infection
(reviewed in Banchereau et al22).
One family of infection-induced cytokines that can activate DCs is the
type I interferons (type I IFNs). Type I IFNs include a number of
evolutionarily conserved proteins encoded by closely related and linked
genes, the major species of which are IFN- Evidence that type I IFNs can activate DCs has come from studies on DCs
generated in vitro from peripheral blood or bone marrow precursor
cells. In these models, the general finding has been that addition of
type I IFNs to mouse8 or human30-34 DCs
enhanced their expression of costimulatory molecules and ability to
stimulate T cells, although there is also a report that type I IFNs can have the opposite effect.35 The ability of type I IFNs to
activate DCs is interesting given that these cells can also produce
type I IFNs in response to infection. Thus, it has been reported that type I IFNs are secreted by human DC precursors,28,36 in
vitro-derived human DCs,15 and murine splenic
DCs37 in response to pathogen-associated signals. In
addition, there is some evidence that the DC-secreted type I IFNs can
act in an autocrine manner, promoting survival of DC
precursors29 and simulating expression of type I
IFN-induced genes in activated human DCs.15,38 These
findings therefore raise the question of whether type I IFN can also
serve as an autocrine factor for DC activation.
In this study, we have examined the ability of in vivo- or in
vitro-generated DCs to secrete and respond to type I IFN. We report
that murine splenic DCs (sDCs), like in vitro-derived DCs, undergo
maturation after treatment with type I IFN in vivo or in vitro.
Furthermore, both sDCs assayed immediately ex vivo and DCs generated
from bone marrow precursors in vitro (BM-DCs) express IFN- Mice
DC isolation and culture
The sDCs were obtained with the use of a method based on that described
by Vremec et al.44 In brief, spleens from 6 to 8 mice were
pooled and cut into small fragments. The homogenate was digested in
RPMI 1640 medium containing 10% heat-inactivated FCS, 1 mg/mL Type III
collagenase (Worthington Biochemical, Lorne Laboratories,
Twyford, Reading, United Kingdom), and 325 U/mL DNase I
(Sigma-Aldrich) by mixing for 25 minutes at room temperature. Then 0.6 mL of 0.1 M EDTA, pH 7.2, was added for an additional 5 minutes, to allow disruption of DC-T-cell complexes. Cells were pelleted, resuspended in 1.077 g/mL Nycodenz (Life Technologies), layered on Nycodenz, and centrifuged in a Sorval RT7plus centrifuge at
2000g for 20 minutes. The low-density fraction was collected and incubated on ice with anti-CD11c fluorescein isothiocyanate (FITC)
monoclonal antibody (Pharmingen, Becton Dickinson UK, Cowley, Oxford)
followed by incubation with anti-FITC Microbeads (Miltenyi Biotech,
Bisley, Surrey, United Kingdom) for 20 and 15 minutes, respectively.
The positive fraction was recovered by passing over a MACS separation
column (Miltenyi Biotech) and checked on a FACSCalibur (Becton
Dickinson UK) for purity; 93% to 98% purity was routinely attained.
Cells were then plated at 1 × 106/mL in IMDM
containing 10% heat-inactivated FCS, 50 µM 2-ME, 100 U/mL
penicillin, 100 µg/mL streptomycin, and 100 U/mL polymyxin B in the
presence or absence of 1000 neutralizing units of antimouse IFN- Flow cytometric analysis The following monoclonal antibodies (all from Pharmingen) were used: anti-CD54 (ICAM-1) biotin (3E2), anti-CD40 biotin (HM40-3), anti-CD80 (B7-1) biotin (16-10A1), anti-CD87 (B7-2) biotin (GL1), anti-H2Db-biotin (28-14-8), anti-I-Ad/I-Ed-biotin (2G9), anti-CD11c (HL3), used as FITC or biotin. Biotinylated monoclonal antibodies were detected with streptavidin-Red 670 (Life Technologies) or streptavidin-Cy5 (TCS Biologicals, Botolph Claydon, Buckinghamshire, United Kingdom). Aliquots of 2 to 5 × 105 cells were stained in phosphate-buffered saline (PBS), 2% FCS, and 0.1% NaN3 and analyzed on a FACScalibur with the use of the CellQuest software (Becton Dickinson UK).Reverse transcriptase-polymerase chain reaction and analysis of amplified products Messenger RNA (mRNA) was purified from 2 × 106 CD11c+ sDCs or BM-DCs by means of a Quickprep Micro mRNA purification kit (Amersham Pharmacia Biotech UK). Then, 500 ng mRNA was incubated for 10 minutes with Oligo-p(dT)15 primers (Boehringer Mannheim UK, Lewes, East Sussex) at 25°C in the presence of 50 U RNAse inhibitors (Boehringer Mannheim UK) and reverse transcribed with 20 U AMV reverse transcriptase (Boehringer Mannheim UK) for 1 hour at 42°C in a final volume of 20 µL (10 mM Tris, 50 mM KCl, 5 mM MgCl2, 1 mM deoxynucleoside-nucleoside 5'-triphosphates [dNTPs]; pH 8.3). In some experiments, total RNA was extracted by means of a miniprep total RNA purification kit (Qiagen, Crawly, West Sussex, United Kingdom). In this case, an "on-column" digestion with DNase I (Qiagen) was performed. RNA so obtained was then reverse transcribed by means of Oligo-p(dT)15 primers to select polyadenylated RNA (ie, mRNA). Polymerase chain reaction (PCR) was performed on 2 µL each complementary DNA (cDNA) sample or, as controls, either 2 µL sterile water or 2 µL total RNA that had not been reverse transcribed, by means of 1.25 U Thermoprime Plus DNA polymerase (Advanced Biotechnologies, Epson, Surrey, United Kingdom) in a final volume of 50 µL containing 75 mM Tris-HCl, 20 mM ammonium persulfate, 0.1% Tween 20, 1.5 mM MgCl2, 0.2 mM dNTPs, 10 pmol sense primer, and 10 pmol antisense primer at pH 8.8. Primers used were the following: murine IFN- 1/IFN-2, 5'-TGTCTGATGCAGCAGGTGG-3' (sense),
5'-AAGACAGGGCTCTCCAGAC-3' (antisense); murine IFN- , 5'-CCATCCAAGAGATGCTCCAG-3' (sense), 5'-GTGGAGAGCAGTTGAGGACA-3' (antisense); -actin, 5'-TGACGGGGTCACCCACACTGTGCCCATCTA-3'
(sense), 5'-CTAGAAGCATTGCGGTGGAGCATGGAGGG-3' (antisense). All primers
were obtained from Life Technologies. Samples were amplified under the
following PCR conditions: 40 seconds denaturation at 94°C, 40 seconds
annealing at 62°C, and 1 minute extension at 72°C (40 cycles for
IFN-1/IFN-2 and IFN-, 25 to 30 cycles for -actin). Samples
were then further incubated at 72°C for 5 minutes. Amplified products
(10 µL) were then separated by agarose gel electrophoresis on a 1.2%
Tris-acetate ethylenediamine-tetraacetic acid gel and visualized by ethidium bromide staining and UV transillumination.
IFN bioassay First, 106 DCs were plated in each well of a 96-well culture plate in a volume of 200 µL, in the presence or absence of 1000 neutralizing units of antimouse IFN- sheep immunoglobulin.
Cultures were incubated at 37°C in 5% CO2 for 18 hours,
after which the supernatant was harvested. We assayed 50 or 100 µL of
each sample for IFN- biological activity by measuring its ability
to confer resistance to encephalomyelocarditis virus infection upon
L929 cells as described elsewhere.46 The activity of the
supernatants was determined by comparison with that of rIFN- (ICN
Pharmaceuticals, Basingstoke, Hampshire, United Kingdom). Each unit, as
expressed in the text, represents 4 international IFN units.
Proliferation assays DCs were irradiated (2500 radions) and plated in RPMI 1640 medium supplemented with 7% heat-inactivated FCS, 50 µM 2-ME, 100 U/mL penicillin, 100 µg/mL streptomycin, and 100 U/mL polymyxin B at the indicated numbers per well in 96-well flat-bottomed culture plates. Then, 2 × 105 responder cells were added per well. CD4+ responder T cells were positively selected from the lymph nodes of DO11.10 mice.41 Briefly, lymph nodes were pooled, gently cut into small fragments, and digested in collagenase/DNase as described above. Cells were washed and incubated with anti-CD4 microbeads (Miltenyi Biotech), and the positive fraction was collected by passing cells through a MACS column (Miltenyi Biotech). This population was subsequently incubated with a monoclonal antibody to mouse TCR clonotype (KJ1-26-FITC) (Caltag Laboratories, TCS Biologicals), and the labeled cells were sorted on a MoFlo flow cytometer (Cytomation, Fort Collins, CO). CD8+ responder T cells were isolated from 2C TCR transgenic mice40 by positive selection with antimouse CD8 microbeads (Miltenyi Biotech). The purity of the responder cell populations was checked by
FACS analysis and ranged from 90% to 98%. Agonistic peptides (synthesized in the Institute for Animal Health) were added at the indicated concentrations. For DO11.10 responder cells, the peptide
corresponding to amino acids (aa) 323 through 339 of ovalbumin, which
can be presented by I-Ad or I-Ab, was
used,47 while for 2C responder cells, the
synthetic peptide Ser-Ile-Tyr-Arg-Tyr-Tyr-Gly-Leu, which is
presented on Kb (Kb = H  2Kb),48 was used. At 4 days
after the cells were placed in culture, plates were pulsed for 16 hours
with 3H-thymidine (1 µCi [37 KBq] per well).
Incorporation of 3H-thymidine into DNA was analyzed
following cell harvesting by liquid scintillation counting.
Interferons High-titer IFN- was prepared in the C243-3 cell line
following a method adapted from Tovey et al46 Briefly,
confluent cells were primed by the addition of 10 U/mL IFN in Eagle
minimum essential medium (MEM) enriched with 10% FCS and 1 mM sodium
butyrate. After 16 hours of culture at 37° C, C243-3 cells were
infected by Newcastle disease virus (multiplicity of infection of 1) in MEM plus 0.5% FCS plus 5 mM theophylline. At 18 hours after infection, culture supernatant was collected and centrifuged at 1500 rpm for 10 minutes. The supernatant was adjusted to pH 2.0 and kept at 0°C for 6 days. IFN was concentrated and partially purified by ammonium sulfate
precipitations and dialysis against PBS, followed by further dialysis
for 24 hours at 4°C against 0.01 M percloric acid and then against
PBS, before being tested for any possible residual toxicity on a line
of L1210 cells resistant to IFN. These partially purified IFN
preparations had a titer of at least 2 × 107 U/mg of
protein and were endotoxin free, as assessed by the Limulus amebocyte assay.
For injections, either 1 × 105 U IFN- Cytokine detection assays First, 106 purified sDCs cells were plated in each well of a 96-well culture plate in a volume of 200 µL, in the presence or absence of 1000 neutralizing units of antimouse IFN-
sheep immunoglobulin.
Cultures were incubated at 37°C, in 5% CO2 for 18 hours,
after which supernatant was collected and titers of IFN- Confocal analysis Splenic DCs were purified from B6 mice, incubated for 1 hour at 37° C in IMDM containing GolgiPlug (Pharmingen), placed on microscope slides, and fixed with an acetone-to-ethanol ratio of 1:1. Fixed cells were stained primarily with biotin-conjugated hamster antimouse CD11c (HL3) and rat antimouse IFN- (Alexis, Nottingham, United Kingdom) or
with isotype-matched controls. Primary antibodies were detected with
streptavidin-Cy5 and FITC-conjugated antirat immunoglobulin  chain
(MRK-1, Pharmingen), respectively. Cells were analyzed on a Leica
TCS-NT confocal system (Milton Keynes, United Kingdom).
Role of type I IFN in DCs maturation from bone marrow precursors Cells exhibiting the surface markers and functional properties of mature DCs can be generated in vitro by culturing mouse bone marrow cells in the presence of GM-CSF.42,43 This in vitro culture system was used as an initial approach both to assess the expression of type I IFN in DCs and to determine whether type I IFNs play a role in DC maturation. Cells expressing the CD11c marker indicative of DCs were present as early as 6 days after initiating the culture. Approximately 60% to 72% of the cells were CD11c+ at this time (data not shown), and this increased to about 90% by day 14 (Figure 1). To determine whether these BM-DCs were expressing type I IFN, CD11c+ cells from day-6 cultures were purified by means of MACS beads, and mRNA was extracted for reverse transcriptase (RT)-PCR analysis. With the use of primers specific for IFN- (subtypes 1 and
2) and IFN-, it was apparent that both IFN- and IFN-
were expressed in these cells (Figure
2A). Expression of type I IFN at the
protein level was also assessed by means of a bioassay that detects the presence of antiviral activity.46 In this experiment,
day-12 CD11c+ BM-DCs were washed and incubated for 18 hours, after which the supernatant was collected. As shown in Table
1, this supernatant contained IFN-/
activity, demonstrating that BM-DCs were both producing and secreting
type I IFN.
To determine whether the IFN- The less activated phenotype of type I IFN-R KO BM-DCs suggested that
these cells may also have a reduced ability to act as APCs. To assess
this possibility, type I IFN-R KO and control BM-DCs were tested for
their ability to present peptides to naive antigen-specific T cells
derived from TCR transgenic mice. Responder CD8+ T cells
were purified from 2C TCR transgenic mice; these cells recognize an
8-aa peptide (Ser-Ile-Tyr-Arg-Tyr-Tyr-Gly-Leu) in association with
Kb.48 As shown in Figure
3, type I IFN-R KO BM-DCs were much less potent APCs than control BM-DCs for the induction of CD8+
T-cell proliferation. Approximately 4 times as many type I IFN-R KO
BM-DCs were required to induce a response similar to that elicited by
control BM-DCs (Figure 3A). Furthermore, an equivalent number of
control BM-DCs were able to induce significant T-cell proliferation at
about a 15-fold lower peptide concentration (Figure 3B). Type I IFN-R
KO BM-DCs were also less efficient than control BM-DCs in presenting
peptides to CD4+ T cells, although the differences were
less dramatic than for presentation to CD8+ T cells (Figure
3C). Here, using ovalbumin peptide-specific (aa 323 through 339)
DO11.10 T cells41 as responders, it was found that control
BM-DCs did stimulate greater proliferation than type I IFN-R KO BM-DCs,
but only when DCs were present in low numbers (6250 BM-DCs per well).
These results therefore show that although BM-DCs can be generated in
the absence of signaling via type I IFN, these DCs are phenotypically
and functionally less mature than those produced from precursors
responsive to type I IFN.
Role of type I IFNs in sDC activation The observation that BM-DCs both secrete and respond to type I IFN raised the question of whether DCs that arise in vivo behave in a similar way. To determine whether in vivo-generated DCs respond to type I IFN, we examined the phenotype of sDCs isolated from mice that had been injected with IFN-/ 4 hours previously (Figure 4A). Compared with control sDCs, sDCs
from IFN-/-injected mice exhibited increased cell surface
expression of CD40 and CD86, indicating that they had been activated in
vivo. Similar phenotypic changes occurred when IFN-/ was added to
purified sDCs during overnight culture (Figure 4B). In this case,
assessment of the effect of IFN-/ was complicated by the fact
that "spontaneous" phenotypic activation of sDCs occurred upon
placing these cells in culture in the absence of added IFN-/ (see
below). Nevertheless, the in vitro results showed that type I IFN could
act directly on sDCs to stimulate activation.
Having shown that sDCs respond to type I IFN, we then determined
whether DCs isolated from the spleens of normal mice expressed type I
IFN. As shown in Figure 2B, mRNA for both IFN-
Overnight culture of sDCs was associated with phenotypic activation.
Thus, sDCs cultured for 18 hours in medium alone had markedly higher
surface expression of CD40, CD80, CD86, MHC class I, and MHC class II
compared with sDCs examined directly ex vivo (Figure
6A, and data not shown). These
differences were seen on both the CD8+ and the
CD8
Anti-IFN-
To determine whether the DC-secreted type I IFN affected the functional
status of sDCs, cells cultured for 18 hours in the presence or absence
of anti-IFN-
Up-regulation of expression of type I IFN is one of the earliest cellular responses upon contact with infectious agents. The rapid induction of type I IFN reflects the crucial role that these cytokines play in the inhibition of viral spread before the generation of a specific immune response. Indeed, type I IFNs were identified and named on the basis of their ability to confer an antiviral state on target cells, and much is now known about the mechanisms by which they achieve this.49 However, the timing of their expression also makes type I IFNs ideal signaling molecules for alerting the immune system to the presence of infection. This aspect of the activity of type I IFNs has also been recognized for many years, particularly with regard to their stimulatory effects on natural killer (NK) cells and macrophages.50-52 More recently, the development of techniques for generating DCs in vitro has allowed for an assessment of the effects of type I IFNs on these key regulators of the immune response. Consistent with a role in linking innate and adaptive immunity, treatment with type I IFNs has been shown to activate in vitro-derived DCs, enhancing and modulating their ability to initiate T-cell responses.8,30-34 More recently, it has been shown that type I IFNs promote antibody responses in vivo and that stimulation of DCs by type I IFNs plays a role in this adjuvant activity.53 In the present study, we have demonstrated that type I IFNs are in fact autocrine activation factors for in vitro- and in vivo-derived DCs, both of which secrete and respond to type I IFNs. Type I IFNs were expressed not only by BM-DCs but also by DCs immediately after their isolation from spleen. The latter expression implies that type I IFNs are expressed by sDCs in situ, although one cannot formally exclude the possibility that expression was induced during the DC-isolation procedure. In situ expression of type I IFNs by sDCs could reflect in vivo contact with environmental microbes, or components thereof, which may have occurred either in the spleen or in peripheral tissues prior to migration of the DCs to the spleen. Conversely, DC expression of type I IFNs may be independent of stimuli derived from infectious agents. This possibility is worth considering, since it has been shown that type I IFNs are expressed constitutively by resting macrophages.25,54,55 Analogous to the role of type I IFNs in macrophages,55,56 a function of the background expression of these IFNs might be to confer a baseline level of resistance to virus infection on DCs. This baseline resistance could, for example, be crucial in preventing depletion of APCs by rapidly acting lytic viruses. However, the question of whether background expression of type I IFNs by DCs is independent of exposure to micro-organisms will require an analysis of DCs from axenic mice. Regardless of the factors driving DC secretion of type I IFNs, we have
shown here that these cytokines can act in an autocrine manner to
activate DCs. Thus, a reduced state of activation was observed for DCs
generated in vitro from the bone marrow of type I IFN-R KO mice and for
sDCs isolated from normal mice and cultured in the presence of a
neutralizing anti-IFN- The precise reason for the reduced ability of DCs matured in the
absence of signaling by type I IFN to present peptides to T cells is
unknown. Although there were lower levels of surface MHC class II on
type I IFN-R KO BM-DCs and class I on sDCs cultured with
anti-IFN- In recent years, it has become apparent that IFN-
The authors thank Nicola Colburn and Andrew Worth for cell sorting and technical assistance with flow cytometric and confocal analysis.
Submitted July 27, 2001; accepted December 17, 2001.
Supported by the Edward Jenner Institute for Vaccine Research, the European Community (contract no. QLK2-CT-2001-02103 and Associazione Italiana per la Ricerca sul Cancro, Fasc n D5A), and a grant from the Italian Ministry of Health on "Cytokines as vaccine adjuvants." This is publication no. 27 from the Edward Jenner Institute for Vaccine Research.
M.M. and G.S. contributed equally to this work.
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: David F. Tough, The Edward Jenner Institute for Vaccine Research, Compton, Newbury, Berkshire RG20 7NN, United Kingdom; e-mail: david.tough{at}jenner.ac.uk.
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C. D. Conrady, M. Thapa, T. Wuest, and D. J. J. Carr Loss of Mandibular Lymph Node Integrity Is Associated with an Increase in Sensitivity to HSV-1 Infection in CD118-Deficient Mice J. Immunol., March 15, 2009; 182(6): 3678 - 3687. [Abstract] [Full Text] [PDF]
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J. Louten, N. van Rooijen, and C. A. Biron Type 1 IFN Deficiency in the Absence of Normal Splenic Architecture during Lymphocytic Choriomeningitis Virus Infection. J. Immunol., September 1, 2006; 177(5): 3266 - 3272. [Abstract] [Full Text] [PDF]
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A. Sato, M. Ohtsuki, M. Hata, E. Kobayashi, and T. Murakami Antitumor Activity of IFN-{lambda} in Murine Tumor Models. J. Immunol., June 15, 2006; 176(12): 7686 - 7694. [Abstract] [Full Text] [PDF]
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M. Severa, M. E. Remoli, E. Giacomini, J. Ragimbeau, R. Lande, G. Uze, S. Pellegrini, and E. M. Coccia Differential responsiveness to IFN-{alpha} and IFN-{beta} of human mature DC through modulation of IFNAR expression J. Leukoc. Biol., June 1, 2006; 79(6): 1286 - 1294. [Abstract] [Full Text] [PDF]
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C. B. Lopez, J. S. Yount, T. Hermesh, and T. M. Moran Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons J. Virol., May 1, 2006; 80(9): 4538 - 4545. [Abstract] [Full Text] [PDF]
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N. Gerlach, S. Schimmer, S. Weiss, U. Kalinke, and U. Dittmer Effects of type I interferons on friend retrovirus infection. J. Virol., April 1, 2006; 80(7): 3438 - 3444. [Abstract] [Full Text] [PDF]
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M. J. Edwards, O. Buchatska, M. Ashton, M. Montoya, Q. D. Bickle, and P. Borrow Reciprocal Immunomodulation in a Schistosome and Hepatotropic Virus Coinfection Model J. Immunol., November 15, 2005; 175(10): 6275 - 6285. [Abstract] [Full Text] [PDF]
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M. Sundquist and M. J. Wick TNF-{alpha}-Dependent and -Independent Maturation of Dendritic Cells and Recruited CD11cintCD11b+ Cells during Oral Salmonella Infection J. Immunol., September 1, 2005; 175(5): 3287 - 3298. [Abstract] [Full Text] [PDF]
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A. S. Hidmark, G. M. McInerney, E. K. L. Nordstrom, I. Douagi, K. M. Werner, P. Liljestrom, and G. B. K. Hedestam Early Alpha/Beta Interferon Production by Myeloid Dendritic Cells in Response to UV-Inactivated Virus Requires Viral Entry and Interferon Regulatory Factor 3 but Not MyD88 J. Virol., August 15, 2005; 79(16): 10376 - 10385. [Abstract] [Full Text] [PDF]
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S. S. Pejawar, G. D. Parks, and M. A. Alexander-Miller Abortive versus Productive Viral Infection of Dendritic Cells with a Paramyxovirus Results in Differential Upregulation of Select Costimulatory Molecules J. Virol., June 15, 2005; 79(12): 7544 - 7557. [Abstract] [Full Text] [PDF]
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E. M. Bautista, G. S. Ferman, D. Gregg, M. C. S. Brum, M. J. Grubman, and W. T. Golde Constitutive Expression of Alpha Interferon by Skin Dendritic Cells Confers Resistance to Infection by Foot-and-Mouth Disease Virus J. Virol., April 15, 2005; 79(8): 4838 - 4847. [Abstract] [Full Text] [PDF]
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M. Montoya, M. J. Edwards, D. M. Reid, and P. Borrow Rapid Activation of Spleen Dendritic Cell Subsets following Lymphocytic Choriomeningitis Virus Infection of Mice: Analysis of the Involvement of Type 1 IFN J. Immunol., February 15, 2005; 174(4): 1851 - 1861. [Abstract] [Full Text] [PDF]
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A. S. McKee, F. Dzierszinski, M. Boes, D. S. Roos, and E. J. Pearce Functional Inactivation of Immature Dendritic Cells by the Intracellular Parasite Toxoplasma gondii J. Immunol., August 15, 2004; 173(4): 2632 - 2640. [Abstract] [Full Text] [PDF]
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K. L. Brzoza, A. B. Rockel, and E. M. Hiltbold Cytoplasmic Entry of Listeria monocytogenes Enhances Dendritic Cell Maturation and T Cell Differentiation and Function J. Immunol., August 15, 2004; 173(4): 2641 - 2651. [Abstract] [Full Text] [PDF]
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G. Schiavoni, C. Mauri, D. Carlei, F. Belardelli, M. Castellani Pastoris, and E. Proietti Type I IFN Protects Permissive Macrophages from Legionella pneumophila Infection through an IFN-{gamma}-Independent Pathway J. Immunol., July 15, 2004; 173(2): 1266 - 1275. [Abstract] [Full Text] [PDF]
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M. Franchini, H. Hefti, S. Vollstedt, B. Glanzmann, M. Riesen, M. Ackermann, P. Chaplin, K. Shortman, and M. Suter Dendritic Cells from Mice Neonatally Vaccinated with Modified Vaccinia Virus Ankara Transfer Resistance against Herpes Simplex Virus Type I to Naive One-Week-Old Mice J. Immunol., May 15, 2004; 172(10): 6304 - 6312. [Abstract] [Full Text] [PDF]
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G. Schiavoni, F. Mattei, P. Borghi, P. Sestili, M. Venditti, H. C. Morse III, F. Belardelli, and L. Gabriele ICSBP is critically involved in the normal development and trafficking of Langerhans cells and dermal dendritic cells Blood, March 15, 2004; 103(6): 2221 - 2228. [Abstract] [Full Text] [PDF]
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L. Gabriele, P. Borghi, C. Rozera, P. Sestili, M. Andreotti, A. Guarini, E. Montefusco, R. Foa, and F. Belardelli IFN-{alpha} promotes the rapid differentiation of monocytes from patients with chronic myeloid leukemia into activated dendritic cells tuned to undergo full maturation after LPS treatment Blood, February 1, 2004; 103(3): 980 - 987. [Abstract] [Full Text] [PDF]
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 V. van Pesch and T. Michiels Characterization of Interferon-{alpha} 13, a Novel Constitutive Murine Interferon-{alpha} Subtype J. Biol. Chem., November 21, 2003; 278(47): 46321 - 46328. [Abstract] [Full Text] [PDF]
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J. A. Murphy, R. J. Duerst, T. J. Smith, and L. A. Morrison Herpes Simplex Virus Type 2 Virion Host Shutoff Protein Regulates Alpha/Beta Interferon but Not Adaptive Immune Responses during Primary Infection In Vivo J. Virol., September 1, 2003; 77(17): 9337 - 9345. [Abstract] [Full Text] [PDF]
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 F. Moschella, B. Bisikirska, A. Maffei, K. P. Papadopoulos, D. Skerrett, Z. Liu, C. S. Hesdorffer, and P. E. Harris Gene Expression Profiling and Functional Activity of Human Dendritic Cells Induced with IFN-{alpha}-2b: Implications for Cancer Immunotherapy Clin. Cancer Res., June 1, 2003; 9(6): 2022 - 2031. [Abstract] [Full Text] [PDF]
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T. K. Means, F. Hayashi, K. D. Smith, A. Aderem, and A. D. Luster The Toll-Like Receptor 5 Stimulus Bacterial Flagellin Induces Maturation and Chemokine Production in Human Dendritic Cells J. Immunol., May 15, 2003; 170(10): 5165 - 5175. [Abstract] [Full Text] [PDF]
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M. Dalod, T. Hamilton, R. Salomon, T. P. Salazar-Mather, S. C. Henry, J. D. Hamilton, and C. A. Biron Dendritic Cell Responses to Early Murine Cytomegalovirus Infection: Subset Functional Specialization and Differential Regulation by Interferon {alpha}/{beta} J. Exp. Med., April 7, 2003; 197(7): 885 - 898. [Abstract] [Full Text] [PDF]
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P. Brawand, D. R. Fitzpatrick, B. W. Greenfield, K. Brasel, C. R. Maliszewski, and T. De Smedt Murine Plasmacytoid Pre-Dendritic Cells Generated from Flt3 Ligand-Supplemented Bone Marrow Cultures Are Immature APCs J. Immunol., December 15, 2002; 169(12): 6711 - 6719. [Abstract] [Full Text] [PDF]
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G. Schiavoni, F. Mattei, P. Sestili, P. Borghi, M. Venditti, H. C. Morse III, F. Belardelli, and L. Gabriele ICSBP Is Essential for the Development of Mouse Type I Interferon-producing Cells and for the Generation and Activation of CD8{alpha}+ Dendritic Cells J. Exp. Med., December 2, 2002; 196(11): 1415 - 1425. [Abstract] [Full Text] [PDF]
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Top
Abstract
Introduction
, and T-cell stimulatory activity. These results
show that DCs both secrete and respond to type I IFN, identifying type
I interferons as autocrine DC activators.
(Blood. 2002;99:3263-3271)
subsets of sDCs (data not shown). Since the sDCs were
actively secreting type I IFN into the supernatant during this time,
the question arose as to whether the phenotypic changes were due to autocrine/paracrine activation by type I IFN. To address this question,
the activity of type I IFN was blocked by adding neutralizing anti-IFN-
