Yonago Acta medica 1999;42:1–10

Expression of Surface Markers on Mature Monocyte-Derived Dendritic
Cells from Allergic Asthmatics
Hiroki Yajima, Katsuyuki Tomita and Yutaka Hitsuda
Third Department of Internal Medicine, Faculty of Medicine, Tottori University, Yonago
683-0826, Japan
Dendritic cells (DCs) are one type of important inflammatory cells in the pathogenesisof asthma for early response to allergen exposure. Monocyte-derived DCs (MoDCs)
are characterized by a high antigen uptake capacity and poor T-cell stimulatory activity,
both features of immature DCs. By stimulation with tumor necrosis factor-α (TNF-α)
or antigen capture, these cells differentiate into mature DCs with the disappearance ofantigen-capturing regions, and increase in stimulatory activity. We measured the expression of some molecules on MoDCs before and after stimulation with TNF-α or house
dust mite (HDM) antigen, from 9 house dust mite (HDM)-allergic asthmatic patientsand 8 normal control subjects by flow cytometry. Primary MoDCs from HDM-allergic
asthmatics showed a greater expression of histocompatibility leukocyte antigen (HLA)DR and mannose receptor (MR), but not of CD80, CD86 or intercellular adhesion
molecule-1 (ICAM-1), than those from normal subjects (P < 0.05). After stimulation
with TNF-α or HDM, DCs from asthmatic patients showed a greater expression of
HLA-DR, CD86 and ICAM-1, than those from normal subjects. In HDM-allergic
asthmatic patients, MR expression on DCs significantly declined after stimulation by
HDM compared with stimulation by TNF-α (P < 0.05). Results suggest that the reductionof MR expression may be characteristic on mature DCs after HDM exposure in allergic
asthma.
Key words: asthma; dendritic cells; histocompatibility leukocyte antigen-deoxyribose; house dust
mite; mannose receptor

Allergic asthma is a chronic inflammatory
disease characterized by increased infiltrationof eosinophils and allergen-specific Th2 lymphocytes into the airways (Lundgren et al.,
1988; Ackerman et al., 1994). It is generally
accepted that airway dendritic cells (DCs) areessential for stimulating naive T cells in a primary immune response to inhaled antigens andthe most prominent cells involved in thepresentation of inhaled antigens to Th2 lymphocytes (Ackerman et al., 1994; Bellini et al.,
1993; Inaba et al., 1990). DCs are present in

the bronchial mucosa of both normal and asthmatic subjects. As assessed by immunohistochemistry, the airways of atopic asthmatics are
known to contain increased numbers of CD1a +DCs (Moller et al., 1996).
The DC population in the airway epithelium
is renewed every 48 to 72 h; a more rapid
turnover reveals that DCs originate in the bonemarrow and supposedly belong to the monocyte
lineage (Holt et al., 1994; McWilliam et al.,1995). Romani and colleagues (1994) recently
demonstrated that monocyte-enriched periph-

Abbreviations: DC, dendritic cell; FEV1.0, forced expiratory volume in one second; FITC, fluorescein
isothiocyanate; GM-CSF, granulocyte-macrophage colony-stimulating factor; HDM, house dust mite; HLA,
histocompatibility leukocyte antigen; ICAM-1, intercellular adhesion molecule-1; IgE, immunoglobulin E;
IL-4, interleukin-4; MHC, major histocompatibility complex; MoDC, monocyte-derived dendritic cell; MR,mannose receptor; PBMC, peripheral blood mononuclear cell; PBS, phosphate buffered saline; TNF-α, tumor
necrosis factor-α

1

H. Yajima et al.

Table 1. Patients Characteristics
Patient
numberSex

Age(year)

Total serum
IgE(IU/mL)

Minimum
dose ofmethacholine (U)FEV1.0(% predicted)

1
Male
16
4300
80.9
3.387
2
Male
23
289
84.5
0.206
3
Male
24
1045
91.5
1.045
4
Male
30
11200
79.6
0.049
5
Male
34
170
89.3
1.358
6
Male
37
246
74.1
0.439
7
Female
19
2650
82.5
2.13
8
Female
22
6060
77.2
0.459
9
Female
26
1125
70.1
ND
FEV1.0, forced expiratory volume in one second; IgE, immunoglobulin E; ND, not done.

eral blood mononuclear cells (PBMCs) cultured
with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-4 candifferentiate into DCs (MoDCs).
van den Heuvel and colleagues (1998) reported that MoDCs from allergic asthmatics
showed phenotypic differences in the expression of surface markers. MoDCs have many of
the same features as immature DCs, including
the expression of molecules that enhance antigen capture and weak T-cell stimulation. If
MoDCs are stimulated by tumor necrosis factor-α(TNF-α) or antigens, these cells differentiate
into mature cells with the disappearance ofantigen-capturing regions and an increase in Tcell stimulatory function (Palucka et al., 1998).
It has not been reported whether MoDCs fromasthmatics develop into mature phenotypes
after stimulation with any antigens.
The mannose receptor (MR) is a surface
175-kD C-type lectin and a membrane lectin or
sugar-specific receptor, expressed by macrophages and DCs (Avrameas et al., 1996;
Koning, 1997). MR enhances a histocompatibility leukocyte antigen (HLA) class II-restricted
antigen presentation and specifically mediates
the binding and endocytosis of mannose- andfucose-terminated glycoproteins, which are
involved in the phagocytosis of pathogens suchas the house dust mite (HDM) (Mitra andChatterjee, 1990), because HDM is a complex
of a glycoprotein with a high-mannose type ofoligosaccharide (Uhlir, 1993).

Inhaledbeclomethasone(µg/day)
—
400
400
300
—
—
600
600
600

In this study, we examined the expression of
mature markers and T cell co-stimulating molecules on MoDCs isolated from asthmatics after
stimulation with TNF-α or HDM.

Materials and methods

Subjects
Nine asthmatic patients (6 males and 3 females)
aged 16 to 37 years (mean, 26 years) werestudied (Table 1). Patients with asthma were
defined as having a previous history of episodic
wheezing and reversible airway obstruction,
characterized by an increase in a forced expiratory volume in one second (FEV1.0) of >15%
after inhalation of 40 µg of procaterol. All patients were HDM-allergic, defined by a > 2-mm
wheal response to HDM extract (Torii, Tokyo,
Japan), and a raised serum concentration of
total immunoglobulin E (IgE > 250 IU/mL) or
specific IgE for HDM. None of the patients received oral corticosteroids within the 3 months
preceding the study. Six of the asthmatic subjects were taking regular inhaled corticosteroids(range, 300 to 600 µg of beclomethasone perday). Patients were excluded from the study ifthey experienced an asthmatic attack during the
2 months preceding the study. Eight healthy
volunteers (mean age, 26.4 years; range, 21 to
35 years), who were HDM-non-allergic and had
no history of asthma or allergic diseases, were2

Surface markers on mature DCs from HDM-allergic asthmatics(Romani et al., 1994). In brief, adherent cells(monocyte-enriched peripheral blood mononuclear cells) were cultured in medium supplemented with 800 U/mL of GM-CSF (Genzyme,
Cambridge, MA) and 500 U/mL of IL-4
(Genzyme). Cells were fed every other day(days 2, 4 and 6) with fresh culture medium
containing the same levels of GM-CSF and IL4. On day 7, cells were stimulated with and without 10 µg/mL of HDM extract, supported by
Torri (Tokyo) or 10 ng/mL TNF-α (Genzyme)
for 24 h to induce maturation. At that point, thecells had become mostly non-adherent, andwere removed from the plate and washed twice
in RPMI 1640. They were then counted andanalyzed. Viability was always above 95%.
Cell yields were expressed as the number of
DCs obtained from 108 PBMCs.

studied as a control group. All participating
subjects were non-smokers and had no history
suggesting a viral respiratory tract infection
within 4 weeks preceding or during the study.
All subjects gave their informed consent.

Determination of airway responsivenessAirway response was measured directly byexamining the dose-response curve of respiratory resistance drawn by an Astograph (Chest,
Tokyo) (Takishima et al., 1981) during continuous inhalation of methacholine administeredin a stepwise incremental fashion. Briefly,
methacholine aerosol in doubling concentrations (0.049–100 mg/mL) was inhaled continuously through the mouth during tidal breathingfor each concentration. The aerosol was generated by a micronebulizer (Bird, Palm Springs,
CA) with an output of 0.15 mL/min, and a particle size ranging from 0.5 to 4.0 mm. Assessment of airway responsiveness was derived
from a minimum dose of methacholine needed
to increase the dose-response curve of respiratory resistance.

Immunofluorescence staining
The expression of surface antigens on MoDCs
was determined by the binding of monoclonal
antibodies against CD1a (IgG2a; Cosmo Bio,
Tokyo, Japan), CD1c (IgG1; Cosmo Bio),
HLA-DR (IgG2a; Pharmingen, San Diego,CA), MR (IgG1; Pharmingen), CD80 (IgM;
Serotec, Oxford, United Kingdom), CD86
(IgG1; Serotec), CD54 (IgG1; Coulter, Krefeld,
Germany), CD11b (IgG1; Leinco, Ballwin,MO), CD83 (IgG1; Cosmo Bio), CD14 (IgG2a;
Cosmo Bio), CD16 (IgG1; Nichirei, Tokyo)
and CD3 (IgG1; Leinco) for 90 min on ice.
After the cells were washed 3 times with PBS
containing 0.1% sodium azide (PBS-azide), theexpressions of these surface molecules were
evaluated by indirect fluorescence after incubation for 30 min on ice in the dark with either
fluorescein isothiocyanate (FITC)-conjugatedantibodies (anti-IgG2a, IgG2b, IgM; Cappel,
Durham, United Kingdom) or phycoerythrinconjugated antibodies (anti-IgG1; Southern
Biotechnology, Birmingham, AL). The cells
were washed 4 times with PBS-azide, and wereanalyzed by flow cytometry.

Preparation of DCs
Sixty milliliters of peripheral blood were
sampled from asthmatic patients and normal
subjects. Peripheral blood mononuclear cells(PBMCs) were separated by standard FicollHypaque (specific gravity, 1.077 g/mL;
Pharmacia, Uppsala, Sweden) density gradientcentrifugation, and were washed twice with
Mg2+- and Ca2+-free phosphate buffered saline(PBS, pH 7.4; Research Institute for Medical
Disease, Osaka, Japan). The cells were resuspended in the following medium: RPMI 1640
with 25 mmol/L HEPES and 0.3 mmol/Lglutamine (Bio Whittaker, Walkersville, MD)
containing 10% fetal calf serum (Cansera
International Inc., Rexdale, ON, Canada), 100
U/mL penicillin and 100 µg/mL streptomycin(Bio Whittaker), and then were incubated inculture dishes (Falcon 3002; Becton Dickinson,
San Jose, CA) at 37°C with 5 % CO2 for 1 h.
After non-adherent cells were decanted, DCs
were prepared according to published methods
3

H. Yajima et al.

Flow cytometry
1000

Flow cytometry was performed with 3,000 to
5,000 cells per sample by a FACS Calibur(Becton Dickinson). DCs were analyzed by
selective gating based on forward- and sidescatter parameters with large cells in nonlymphoid areas (Fig. 1). Statistical markers
were set using isotype-matched negative controls.

G1
Side-scatter height

800

600

400

200

Statistical analysis

G2

Statistical analysis was performed with the Stat
View 4.0 statistics package (Abacus Concepts,
Berkeley, CA) and a Power Macintosh 7200/90(Apple Computer, Cupertino, CA). All data areexpressed as the mean + SD. The nonparametric Mann-Whitney U test and Wilcoxon’s
signed-rank test were used for statisticalanalysis of the unpaired data and paired data,
respectively. The rate of induction of relative
fluorescence intensity of MR on MoDCs stimulated with HDM or TNF-α was calculated by
the following formula:

0
0

200

400

600

800

1000

Forward-scatter heightFig. 1. Uniform high forward- and side-scatter
properties of MoDCs (designated G1) and lymphocytes (designated G2) from representative HDMallergic asthmatics (a). HDM, house dust mite; G1,large-cell population; G2, small-cell population;
MoDC, monocyte-derived dendritic cell.

Analysis of DCs by flow cytometry
Figure 1 shows representative forward- versus
side-scatter density plots. On both the forwardand side-scatter, two subpopulations consistingof a large-cell population (G1) and a small-cell
population (G2) were found in the cultured cellswith GM-CSF and IL-4 for 7 days (Fig. 1). The
cells in the small-cell population were CD3positive and CD1a-negative lymphocytes.
Using gating on the large cell population, we
assessed the surface expression on DCs. The
percentages of CD1a- or CD1c-positive cells on
gating on the large-cell population did not differ
between asthmatic patients (48.5 ± 8.3% and81.4 ± 11.3%, respectively) and control subjects (54.5 ± 15.7% and 80.6 ± 10.4%, respectively). Less than 10% of DCs gating on thelarge-cell population expressed CD14.

rFI of MR on MoDCs
stimulated with HDM or TNF-α – 1 × 100
rFI of MR on
non-stimulated MoDCs
where rFI stands for relative fluorescence intensity.

Results

Characteristics of primary MoDCs
To induce primary MoDCs, monocyte-enriched
PBMCs were cultured with GM-CSF and IL-4
for 7 days. The cultured cells were a heterogeneous population containing 16 ± 6% lymphocytes on morphology which was determinedby using May-Grünwald-Giemsa staining.
Whereas 2.9 ± 1.0 × 106 DCs were generated
from 108 PBMCs from normal subjects, 3.8 ±0.7 × 106 DCs could be obtained from PBMC
from HDM-allergic asthmatics compared withnormal subjects (P = 0.05).

Expression of mature markers on DCs
To characterize mature DCs, we have used phenotypes emphasizing the presence of CD83 andHLA-DR. The expression of HLA-DR on primary MoDCs was significantly higher in HDM4

Surface markers on mature DCs from HDM-allergic asthmatics

P = 0.008

Relative fluorescence intensity

800

P = 0.02
P = 0.008*

P = 0.02
600

**
400

*
200

0

Primary
MoDCs+TNF-α+HDMMature MoDCs

Primary
MoDCs

Normal subjects+TNF-α+HDMMature MoDCs

Asthmatic patients

Expression of HLA-DR on MoDCs
Fig. 2. Expression of HLA-DR as a mature marker on MoDCs of asthmatic patients and normal subjects.
Primary MoDCs were derived from plastic-adherent peripheral blood mononuclear cells with 800 U/mL GMCSF and 500 U/mL IL-4 for 7 days. Mature MoDCs were obtained from primary MoDCs by the stimulationof 10 ng/mL TNF-α or 10 µg/mL HDM for 24 h. The lower, middle and upper lines in the boxes represent the
25th, 50th and 75th percentiles, respectively; the lower and upper limits of the bars represent the 10th and 90th
percentiles, respectively. HDM, house dust mite; HLA-DR, histocompatibility leukocyte antigen-DR; IL-4,
interleukin-4; GM-CSF, granulocyte-macrophage colony-stimulating factor; MoDC, monocyte-derived
dendritic cell; TNF-α, tumor necrosis factor-α. *P < 0.05, compared with normal subjects. **P < 0.01,
compared with normal subjects.

allergic asthmatic patients than in normal
subjects (Fig. 2) (P < 0.05), but that of CD83
was not (data not shown). The expression of
CD83 and HLA-DR (Fig. 2) was enhanced after
stimulation with TNF-α or HDM in the samemanner with both asthmatics and control subjects.

higher than that from control subjects (Fig. 3).
There was no remarkable change in the intensity of CD80, or CD11b after stimulation with
TNF-α or HDM in both groups.

Expression of MR on DCs
The expression of MR on primary MoDCs was
significantly higher in HDM-allergic asthmaticpatients than in normal subjects (P < 0.05).
MR expression on MoDCs from HDM-Allergic
asthmatics was significantly reduced bystimulation with HDM as well as TNF-α (Fig.
4). When the rate of induction in the expressionof MR was assessed, the MR of MoDCs fromasthmatics were shown to be more reduced thanthat of DCs from control subjects after stimulation with HDM (P = 0.001) (median reduction
rate; asthmatic subjects, 65% and control subjects, 40%). However, after stimulation with
TNF-α, there was no significant difference

Expression of T cell co-stimulating molecules on DCs
When the expression of T cell co-stimulating
molecules CD80 (B7-1), CD86 (B7-2), CD54
(ICAM-1), and CD11b (Mac-1) on primary
MoDCs was assessed by flow cytometry, thesemolecules did not differ between asthmatics
and control subjects. The expressions of CD54
and CD86 on MoDCs after stimulation with
HDM were increased in the 2 groups of subjects, and the expression of these molecules on
MoDCs from asthmatics was significantly
5

H. Yajima et al.

Relative fluorescence intensityA

P = 0.008

600

P = 0.008

P = 0.02
P = 0.02

*
400

200

0

Primary
MoDCs+TNF-α+HDMMature MoDCs

Primary
MoDCs

Normal subjects+TNF-α+HDMMature MoDCs

Asthmatic patients

Expression of CD54 on MoDCs

B
Relative fluorescence intensity200

P = 0.008

P = 0.02

P = 0.008
160*

P = 0.02

*

120

80

40

0

Primary
MoDCs+TNF-α+HDMMature MoDCs

Primary
MoDCs

Normal subjects+TNF-α+HDMMature MoDCs

Asthmatic patients

Expression of CD86 on MoDCs
Fig. 3. Expression of CD54 (A) and CD86 (B) as T cell co-stimulating molecules on MoDCs of asthmaticpatients and normal subjects. Primary MoDCs were derived from plastic-adherent peripheral bloodmononuclear cells with 800 U/mL GM-CSF and 500 U/mL IL-4 for 7 days. Mature MoDCs were obtained
from primary MoDCs by the stimulation of 10 ng/mL TNF-α or 10 µg/mL HDM for 24 h. The lower, middle
and upper lines in the boxes represent the 25th, 50th and 75th percentiles, respectively; the lower and upper
limits of the bars represent the 10th and 90th percentiles, respectively. HDM, house dust mite; IL-4,
interleukin-4; GM-CSF, granulocyte-macrophage colony-stimulating factor; MoDC, monocyte-derived dendritic cell; TNF-α, tumor necrosis factor-α. *P < 0.05, compared with normal subjects.

6Relative fluorescence intensity

Surface markers on mature DCs from HDM-allergic asthmatics

P = 0.008

P = 0.02300

P = 0.008

P = 0.02

*
200

100

0

Primary
MoDCs+TNF-α+HDMMature MoDCs

Primary
MoDCs

Normal subjects+TNF-α+HDMMature MoDCs

Asthmatic patients

Expression of MR on MoDCs
Fig. 4. Expression of MR on MoDCs of asthmatic patients and normal subjects. Primary MoDCs were
derived from plastic-adherent peripheral blood mononuclear cells with 800 U/mL GM-CSF and 500 U/mL
IL-4 for 7 days. Mature MoDCs were obtained from primary MoDCs by the stimulation of 10 ng/mL TNFα or 10 µg/mL HDM for 24 h. The lower, middle, and upper lines in the boxes represent the 25th, 50th and75th percentiles, respectively; the lower and upper limits of the bars represent the 10th and 90th percentiles,
respectively. HDM, house dust mite; IL-4, interleukin-4; GM-CSF, granulocyte-macrophage colonystimulating factor; MoDC, monocyte-derived dendritic cell; MR, mannose receptor; TNF-α, tumor necrosis
factor-α. *P < 0.05, compared with normal subjects.

between the 2 groups in the rate of reduction of
MR on stimulated MoDCs (median reduction
rate; asthmatic subjects, 55% and control subjects, 75%).

To our knowledge this is the first study ofphenotypical analysis of MoDCs stimulatedwith a specific antigen from allergic asthmatics.
It has been reported that when DCs are induced
to a mature state by TNF-α, CD40L or lipopolysacharide, the expression of MHC class II,
as well as co-stimulatory molecules ICAM-1 andB7, is up-regulated (Sallusto and Lanzavecchia,
1994; Morse et al., 1997; Palucka et al., 1998).
Similarly, our data indicate that MoDCs fromasthmatic patients showed a more maturephenotype after stimulation with HDM thanthose from normal subjects. As to maturephenotypic DCs from asthmatics, 2 reasons
could be considered. First, a mature subpopulation of peripheral monocytes might affect tobe derived into mature-phenotypic DCs fromasthmatics. We have previously shown functional and phenotypic differences between
monocytes from atopic asthmatics and thosefrom normal subjects (Tomita et al., 1995,
1997). Second, exogenous cytokines such as
IL-10, IL-4, GM-CSF or IL-12 might stimulate
DCs to develop into mature cells.

Discussion
We have studied the expression of surface
markers on MoDCs from HDM-allergic asthmatics before and after stimulation with HDM
or TNF-α in vitro. The expressions of HLADR and MR on primary MoDCs from asthmatics was higher than those from normal subjects,
suggesting that these cells from asthmatics weredifferentiated into more mature DCs from thepoint of view of phenotypes as previously demonstrated (van den Heuvel et al., 1998). In
response to HDM, MoDCs from asthmatics
showed a greater expression of HLA-DR,
ICAM-1 and B7-2 than those from normal subjects. In addition, the expression of MR on
MoDCs reduced with stimulation with HDM,
but not TNF-α .
7

H. Yajima et al.

In the airways, DCs are located in and justunderneath the bronchial epithelium to allow
for the uptake of inhaled antigens (Holt et al.,
1997; van Haarst et al., 1994). In most tissues,
DCs are present in a so-called “immature” state,
unable to stimulate T cells. We demonstrated
that immature MoDCs from asthmatic patients
showed a higher expression of HLA-DR thanthose from normal subjects. Furthermore, thisdifferentiated marker was up-regulated bystimulation with HDM as well as TNF-α. A recent study showed that immature DCs wereactive in the biosynthesis of class II MHC andin peptide loading, but the peptide-MHC class
II complexes were recycled by accumulating inlysosomes and reaching the cell surface. If
these cells started to mature, the increased biosynthesis of class II MHC was observed which
maximizes the specific loading of antigens(Cella et al., 1997). So antigen presentation toclass II-restricted T cells generally requires
such newly synthesized class II MHC on mature DCs (Pinet et al., 1995). Thus, our findings
may imply that the newly produced HLA-DR
on “mature” DCs from asthmatics stimulatedwith HDM contributes to the presentation of
inhaled antigens to T cells.
Recent studies have shown that Th2 cells
play an important role in the generation of airway eosinophils in asthma through their ability
to produce IL-5 (Ohnishi et al., 1993; Walker etal., 1994). The depletion of airway DCs suppressed Th2 cytokine-associated eosinophilic
airway inflammation in a mouse model withasthma (Lambrecht et al., 1998) suggesting thatDCs might play an important role in stimulatingTh2 cells. ICAM-1/LFA-1 (King and Katz,
1989) and B7/CD28 (Lenschow et al., 1996;
Reiser and Stadecker, 1996) interactions aremajor pathways for initiating naive T cell activation. DCs treated with TNF-α or lipopolysacharide showed increased expression of theclass II and class I molecules, B7-1 and ICAM1 (Sallusto et al., 1995). Our data demonstrated
that MoDCs from asthmatics treated with TNFα or HDM develop into mature DCs, whichshow enhanced expression of ICAM-1 and B72. Kuchroo and colleagues (1995) reported that

B7-2 was one of the co-stimulating molecules
for signaling Th2 cells.
We also demonstrated a significant reduction in MR on MoDCs from HDM-allergic
asthmatics, after stimulation with HDM but notwith TNF-α, in spite of a lack of significant differences in CD80, CD86 and ICAM-1 expressions. MR, which is expressed on cultured immature DCs (Reis e Sousa et al., 1993; Sallusto
et al., 1995) is internalized to mediate phagocytosis of various microorganisms that expose
mannosylated glycoproteins (Ezekowitz et al.,1991). Indeed, in DCs, MR allows the uptake
and concentration of ligands such as FITClabeled dextran and horseradish peroxidase(Sallusto et al., 1995). Engering and colleagues(1997) demonstrated that the MR pathway in
DCs was ~100-fold more efficient in presenting
antigens to T cells. Upon the maturation of DCs
from HDM-allergic asthmatics, the uptake ofmannosylated antigens such as HDM mightplay an important pathophysiological role inatopic asthma.
We examined the surface expression on
DCs derived from peripheral blood. Airway
DCs originate in peripheral blood monocytes
from the bone marrow (Holt et al., 1994;
McWilliam et al., 1995). McWilliam and colleagues (1995) hypothesized that the location of
the development of DCs from peripheral monocytes after birth may influence the pathogenesisof immune regulated diseases such as asthma
and allergic rhinitis. So, further studies are required to know the nature of MoDCs.
In conclusion, we have shown that immature DCs from patients with allergic asthma
exhibit increased expression of mature markers,
and more extensive development into a maturephase after stimulation with TNF-α or HDM. A
reduction in MR after stimulation with HDM
characterized DCs from patients with HDMallergic asthma. These observations suggestthat MR on “mature” DCs from atopic asthma
might be used to specialize in capturing HDM
antigens.

8Surface markers on mature DCs from HDM-allergic asthmatics

Acknowledgments: The authors wish to thank Prof.
Takao Sasaki, Third Dept. of Internal Medicine,
Faculty of Medicine, Tottori Univ., for his kindadvice and valuable suggestions during the course of
the study. We would also like to thank Prof.
Motoyuki Mihara, Dept. of Dermatology, Faculty of
Medicine, Tottori Univ. and Prof. Shinichi Hayashi,
Dept. Immunology, School of Life Science, Facultyof Medicine, Tottori Univ., for reading this manuscript and giving us helpful suggestions.

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(Received November 4, Accepted November 30,1998)

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