ORIGINAL ARTICLE

HLA-C Expression Pattern Is Spatially Different

between Psoriasis and Eczema Skin Lesions
Lina Carlen1, Kazuko Sakuraba1, Mona Stahle1 and Fabio Sanchez1
Interactions between genetic and environmental factors underlie the immune dysregulation and keratinocyte
abnormalities that characterize psoriasis. Among known psoriasis susceptibility loci (PSORS), PSORS1 on
chromosome 6 has the strongest association to disease. Altered expression of some PSORS1 candidate genes
has been reported but little is known about HLA-C expression in psoriasis. This study compared expression of
major histocompatibility complex class Ia and HLA-C in psoriasis, allergic contact eczema, and normal skin.
Although HLA-C was abundant in protein extracts from both eczema and psoriasis, a consistent and intriguing
difference in the expression pattern was observed; strong immunoreactivity in the basal cell layer, polarized
towards the basement membrane in psoriasis, whereas in eczema lesions HLA-C immunostaining was present
mostly in suprabasal cells. Inflammatory cells in the dermis were strongly stained in both diseases. Normal skin
epithelium showed less intense but similar HLA-C staining as eczema lesions. HLA class Ia expression overall
resembled that of HLA-C in all samples. The distinct HLA-C expression patterns in psoriasis and eczema suggest
a functional role in the specific psoriasis immune response and not only a general feature of inflammation.
Journal of Investigative Dermatology (2007) 127, 342348. doi:10.1038/sj.jid.5700549; published online 28 September 2006

INTRODUCTION
Association between psoriasis and the major histocompatibility complex (MHC) region is firmly established (McMichael et al., 1978; Laurentaci et al., 1982; Henseler and
Christophers, 1985). A minimal genomic segment defining
the psoriasis susceptibility locus 1 (PSORS1) on chromosome
6 (Jenisch et al., 1998; Balendran et al., 1999; Oka et al.,
1999; Nair et al., 2000) contains a number of proposed
candidate genes, for example HLA-C, CDSN (corneodesmosin), CCHCR1 (coiled-coil alpha-helical rod protein 1), SEEK,
and PSORS1C3 (Bowcock and Krueger, 2005). All of them
have been investigated for strength of association to psoriasis
in genetic studies but only some have been studied for
expression in skin (Holm et al., 2003; Suomela et al., 2003;
Capon et al., 2004). There are no published studies that
describe HLA-C expression in psoriasis despite the fact that its
association to disease has been known for several decades.
It is known that under non-inflammatory conditions all
nucleated cells express class I molecules, and that one of
their important functions is to suppress self-reactivity by
engaging inhibitory receptors on natural killer (NK), NK-T
and CD8 cells (Martin and Carrington, 2005; Rajagopalan
1

Dermatology and Venereology Unit, Department of Medicine, Karolinska

Institutet, Stockholm, Sweden
Correspondence: Dr Fabio Sanchez, Molecular Dermatology, CMM L8:02,
Karolinska University Hospital, SE-171 76 Stockholm, Sweden.
E-mail: fabio.sanchez@cmm.ki.se
Abbreviations: KIR, killer cell immunoglobulin-like receptor; MHC, major
histocompatibility complex; NK, natural killer; PSORS, psoriasis
susceptibility locus
Received 22 February 2006; revised 17 May 2006; accepted 22 May 2006;
published online 28 September 2006

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Journal of Investigative Dermatology (2007), Volume 127

and Long, 2005). HLA-C but not HLA-A and B is expressed by

trophoblast where it regulates maternal NK cell reactivity
(Parham, 2004). HLA-C has recently gained attention in
transplantation biology because it has been recognized that
mismatches in the killer immunoglobulin-like receptor (KIR)HLA class I system can lead to transplant rejection (Petersdorf
et al., 1997). This interaction is strongly influenced by the
amino acids present at position 80 and 44 of the HLA-C and
KIR molecules, respectively (Boyington et al., 2001) and is
also influenced by the glycosylation state of the ligands (Baba
et al., 2000). HLA-Cw*0602 has a lysine at position 80 and
interacts mostly with KIRs that possess a methionine at
position 44 (Winter and Long, 1997), such as KIR2DL1
(inhibitory) and KIR2DS1 (activating). Upon interaction,
ligand and receptor are internalized into the effector cell
(Carlin et al., 2001) which is followed by cellular activation
or inhibition (Moretta and Moretta, 2004). HLA-C expression
in the skin has not been described yet, although it is generally
assumed to be low based on expression in other tissues
(McCutcheon et al., 1995).
Although several inflammatory diseases associate with
polymorphisms at MHC class I genes, for example, ankylosing spondylitis with the HLA-B27 allele and subacute
thyroiditis with the HLA-B35 allele (Nyulassy et al., 1977;
Rubin et al., 1994), psoriasis is the only inflammatory disease
that associates with HLA-C (HLA-Cw*0602). The role of
MHC class Ia in the pathophysiological mechanisms of
psoriasis is not well understood; however, it is clear that
inflammation is a marker of disease activity (Krueger and
Bowcock, 2005) and that environmental factors such as
infections can trigger this disease (Wolf and Ruocco, 1999;
Langley et al., 2005), which provides an immunological
& 2006 The Society for Investigative Dermatology

L Carlen et al.
HLA-C Expression Pattern in Psoriasis

playground for HLA-C. In particular, streptococcal throat

infections are often concomitant with onset of guttate
psoriasis, which is the psoriasis subphenotype with the
strongest association to HLA-Cw*0602 (Mallon et al., 2000;
Holm et al., 2005). Whether these associations are circumstantial or do indeed contribute to pathophysiology remains
to be established. In the late 1970s, Gross et al. (1977, 1983)
reported that, in psoriasis, T-cell functions in response to in
vitro exposure to streptococcal factors are influenced by
HLA-C genotypes. No additional reports addressing this
phenomenon are available since then. It is likely that
technical difficulties arising from the high degree of
homology between MHC class I genes and from the high
degree of polymorphism within each gene group explain the
scarcity of studies on this subject. Nonetheless, the role of
HLA-C in immune surveillance (Boyington and Sun, 2002)
and its importance in relation to infection grants a closer look
at its expression pattern in psoriasis.
RESULTS
HLA-C is expressed in skin, tonsil, and adult colon epithelium
but not in fetal colon epithelium

The level and pattern of HLA-C and HLA-ABC expression

were investigated in normal specimens of skin, tonsil, and

colon using antibodies recognizing HLA-C (L31) and

HLA-A,B and C (W6/32). Immunohistochemical analysis
showed that HLA-C staining in tonsil was strong around
germinal follicles and in epithelial cells (Figure 1a). There
was no HLA-C staining in fetal colon epithelium (Figure 1b),
although strong staining in neighboring lymphoid tissue on
the same specimen was evident, in contrast, there was very
strong staining in adult colon epithelium (Figure 1c). HLA-C
expression in normal skin epithelium was predominantly
suprabasal with a membrane-like staining pattern (Figure 1d).
Strong immunoreactivity for HLA-ABC was observed in all
cells, including epithelial cells, in all tissues and in leukocytelike cells, especially large dendritic-like cells (data not
shown), except in fetal colon epithelium where the staining
with this antibody was faint.
Psoriasis and allergic contact eczema skin lesions show spatially
disparate HLA-C expression patterns

Next, we compared the HLA-C expression between plaque

psoriasis, allergic contact eczema, and normal skin. Epidermal HLA-C expression in normal and eczematous tissue was
stronger than in plaque psoriasis. Immunoreactivity in plaque
psoriasis was consistently stronger in the basal layer,
especially at the tips of rete ridges where the signal often

Figure 1. HLA-C expression detected by immunohistochemistry with mAb L31. (a) Tonsil, (b) adult colon epithelium, (c) fetal colon epithelium, (d) normal
skin, (e) plaque psoriasis, (f) allergic contact eczema (original magnification  20, Bar 100 mM, insets:  100, Bar 20 mm) (g) LCL721.221 cells expressing
HLA-Cw3 before lipopolysaccharide stimulation, and after (h) 16, (i) 48, and (j) 96 hours post-stimulation (original magnification  40, Bar 50 mm).

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L Carlen et al.
HLA-C Expression Pattern in Psoriasis

polarized towards the basement membrane (Figure 1e). Clear

pericellular delineation, compatible with membrane staining,
was observed in suprabasal keratinocytes of normal and
allergic contact eczema (Figure 1f). Not all cell types in skin
stained with the L31 anti-HLA-C antibody; fibroblast-like
cells were mostly negative. Leukocyte-like cells as well as
large dendritic-like cells stained strongly with anti-HLA-C in
all sample groups.
MHC class Ia expression was intense and had a similar
distribution pattern to that of HLA-C, showing less intense
staining in the epithelium of plaque psoriasis compared to
normal and eczema skin but with relatively stronger
immunoreactivity in the basal cell layer. An inverse relationship between the number of infiltrating cells and the average
staining density at the basal layer was observed.

a
Expressiom index

1.0

HLA-C protein levels are increased in lesional allergic contact

eczema and plaque psoriasis skin

Using the L31 antibody, a band of approximately 45 kDa,

compatible with the denatured form of HLA-C, was detected
by Western blot in protein extracts from lesional allergic
contact eczema, plaque and guttate psoriasis, non-lesional
samples for these three sample types, and normal skin
samples. The range of HLA-C intensity values among the
different samples was between 0.10 and 1.08 expression
units. Analysis of variance revealed inter-group differences
according to sample category (P 0.0039). Allergic contact
eczema had the most intense HLA-C signal (average
expression index 0.665, standard deviation ( 0.343),
being significantly higher than in the other samples except
for plaque psoriasis (average expression index 0.425,
standard deviation 0.189) (Figure 2a). Overall HLA class I
expression assessed by b2-microglobulin staining was also
increased in allergic contact eczema compared to the other
skin samples (average expression index 0.256, standard
deviation 0.151, P 0.0002) (Figure 2b). A representative
image of an L31-stained membrane is presented in Figure 3.
DISCUSSION
The contribution of the PSORS1 locus to psoriasis susceptibility has been a subject of intense research over the past two
decades (Bowcock and Krueger, 2005). Although several
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Journal of Investigative Dermatology (2007), Volume 127

0.6
0.4
0.2

LE

LG

LP

N
NLE
Phenotype

NLG

NLP

LE

LG

LP

N
NLE
Phenotype

NLG

NLP

0.5

Expressiom index

HLA-C expression on transfected LCL721.221 cells is inducible

with E. coli-derived lipopolysaccharide

In order to determine if HLA-C immunoreactivity correlated

with changes in cellular functional state, LCL721.221 cells,
which lack HLA class I expression, were used. LCL721.221
cells transfected with HLA-Cw3 and Cw4, as well as, nontransfected cells were stimulated with lipopolysaccharide for
up to 96 hours and then tested for reactivity with the L31
antibody. There was a time-dependent increase in the
frequency of L31-positive cells in HLA-Cw3 and Cw4
transfectants, which reached a peak at 48 hours (Figure
1gj). Very faint expression was observed before lipopolysaccharide stimulation for both constructs. No increase in
staining intensity or in the frequency of positive cells was
observed in non-transfected cells at the set time points.

0.8

0.4
0.3
0.2
0.1
0.0

Figure 2. HLA-C protein expression levels in total protein extracts from

psoriasis, eczema and normal skin biopsies. (a) Box plot representation of
HLA-C expression according to sample group, measured by densitometry on
Western blot analysis. (b) Box plot representation of HLA class I expression,
measured by densitometry on Western blot analysis and detected by b2microglobulin staining. LE lesional eczema, LG lesional guttate psoriasis,
LP lesional plaque psoriasis, N normal, NLE non-lesional eczema,
NLG non-lesional guttate psoriasis, NLP non-lesional plaque psoriasis.

45 kDa

b
C NLG LE

LG

LP NLE LP

Figure 3. Representative Western blot membrane showing total protein

smears and specific HLA-C bands. (a) Ponceau staining of the skin protein
extracts after transfer to a membrane. (b) Specific L31 signal. C Control,
LE lesional eczema, LG lesional guttate psoriasis, LP lesional plaque
psoriasis, N normal, NLE non-lesional eczema, NLG non-lesional
guttate psoriasis.

L Carlen et al.
HLA-C Expression Pattern in Psoriasis

genes in this locus are expressed in skin, some with

differential expression between psoriasis and normal skin
(HCR, CDSN), there is no conclusive explanation about their
functional role in psoriasis pathogenesis (Bowcock, 2005).
HLA-C has been considered a susceptibility gene in itself or a
genetic marker in linkage disequilibrium with a psoriasis
gene that has not yet been identified (Helms et al., 2005). If
intrinsic defects in this gene are at the base of psoriasis
pathogenesis then there should be evidence of altered HLA-C
expression or function, otherwise this molecule might
facilitate the effect of third party factors such as autoantigens.
Expression analysis has been critical to understanding the
role of HLA-C in other contexts than psoriasis but with
the common denominator of immune regulatory functions for
this molecule. For example, soluble MHC class I molecules
seem to regulate lymphocyte survival through apoptosis,
tumors can evade immune surveillance by modifying
expression of MHC class I molecules, and HLA-C specifically
contributes to regulate maternal immune reactivity against
fetal tissues (Le Bouteiller, 2001; Puppo et al., 2002; GarciaLora et al., 2003). Global expression studies of RNA and
protein do not indicate differential expression of HLA-C in
psoriasis compared with normal or non-lesional skin (Zhou
et al., 2003; Bowcock, 2005; Carlen et al., 2005), incongruent with HLA-C being a psoriasis susceptibility gene.
However, qualitative as well as quantitative differences are
important in defining the role of HLA-C in psoriasis
pathogenesis. Different patterns of expression can emerge
even in the presence of similar levels of total RNA or protein.
Our findings indicate that HLA-C expression in psoriasis
depends predominantly on infiltrating inflammatory cells,
whereas non-lesional and normal samples express higher
levels of the protein in the epidermis.
It is expected that all nucleated cells express MHC class Ia
molecules because they contribute to preserving peripheral
self tolerance under normal circumstances, that is, no
inflammation, no infection (Zimmer et al., 2005). However,
it is also expected that the constitutive expression of HLA-C
should be low (Neisig et al., 1998). The present study
demonstrated intense staining on infiltrating inflammatory
cells and variable expression levels in the epidermis.
The most striking feature of the HLA-C staining pattern in
this study was the polarization of the signal towards the
basement membrane and the reduced expression on suprabasal keratinocytes in lesional psoriasis samples. It is known
that overexpression of MHC class I molecules can downregulate effector immune cell functions (Parham, 2004);
therefore, reduced expression in psoriasis epithelium might
contribute to maintaining inflammation owing to inefficient
downregulation of activated lymphocytes.
Why would HLA-C be restricted to the basal layer in
psoriasis epidermis? MHC class I clustering into lipid rafts has
been reported as a requirement to binding T-cell receptors
(Lebedeva et al., 2004) and lymphocytes are known to home
towards the skin during psoriasis plaque formation (Davison
et al., 2001), but how these cells interact with the epithelium
is less well documented. HLA-C polarization in psoriasis
epidermis might lead to a directional flow of inflammatory

cells towards the tip of papillae, above which microabscesses

are typically formed (Kaneko et al., 1991). A relevant
observation regarding this possibility is that the inflammatory
infiltrate in psoriasis does not seem to affect the structure of
the basal cell layer, except at the uppermost section of
papillae where HLA-C expression seems lower. In contrast,
the basal cell layer in eczema is characterized by infiltrating
inflammatory cells throughout the epidermis. We attempted
to measure the HLA-C signal intensity at the basal layer of
psoriasis papillae and counted the number of infiltrating cells
through this layer; we observed an inverse relationship
between these variables (data not shown). Since some class
I molecules, including HLA-C, are strong inhibitors of T and
NK cells, the reduced epithelial HLA-C expression might lead
to increased vulnerability to inflammation (Carosella et al.,
2001; Le Discorde et al., 2002; Trowsdale and Betz, 2006),
therefore the polarized HLA-C expression might be a
compensatory mechanism to reduce lymphocyte infiltration.
Support for this view comes from reproduction research
indicating that HLA-C and KIR mismatches appear to fail at
inhibiting NK/NK-T cells in pre-eclampsia, (Hiby et al., 2004;
Parham, 2004). Also in idiopathic bronchiectasis, combinations of HLA-C and KIR associate with the progressive
inflammatory damage to the lungs (Boyton et al., 2006). In
addition, viral regulation of class I gene expression plays a
role in viral persistence; for example, the UL18 protein from
cytomegalovirus can induce HLA-C expression and inhibit
HLA-A and B, which can inhibit antiviral NK/NK-T cell
responses (Gewurz et al., 2001).
There is mounting evidence indicating that immune
surveillance of HLA-C by KIR-positive cells might be a
contributing factor to psoriasis pathogenesis (Martin et al.,
2002; Luszczek et al., 2004; Holm et al., 2005), but
functional studies on this subject are still lacking. However,
it is important to remember that an antigen-driven theory of
psoriasis has been extensively discussed, where HLA-Cw6 is
regarded as a cofactor in the initiation and/or maintenance
of inflammation (Nickoloff et al., 2000; Lin et al., 2001;
Johnston et a.l, 2004).
What would be particular about HLA-Cw*0602 compared
to other HLA-C alleles in this scenario? It is known that HLAC expression varies in relation to the identity of the coding
alleles, but it is not yet known if HLA-Cw*0602 has unique
features that would affect its protein expression. Although this
study does not specifically target the psoriasis-associated
allele HLA-Cw*0602, it shows that HLA-C expression in
normal tissues varies depending on developmental stage and
histological location and reveals that skin epithelium
expresses HLA-C.
The distinct HLA-C expression patterns in psoriasis and
eczema suggest a functional role in the specific psoriasis
immune response and not only a general feature of
inflammation. It will be important to obtain a detailed
description of coding and non-coding sequences of all alleles
in order to identify differences at regulatory sites and design
functional studies that compare HLA-Cw*0602 to other
alleles. This will increase our understanding of the role of
HLA-C in psoriasis pathogenesis.
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HLA-C Expression Pattern in Psoriasis

MATERIALS AND METHODS

Tissue samples
Details regarding patients and controls were reported previously
(Carlen et al., 2005). All study subjects provided written consent and
all research procedures were performed in accordance with the
Declaration of Helsinki Principles and with permission from the
Ethics Committee of the Karolinska Institutet. Biopsies were taken
from lesional and non-lesional skin from guttate and plaque psoriasis
patients, lesional and non-lesional skin from nickel-induced contact
eczema patients, and normal skin of healthy individuals. For
immunohistochemistry, five normal, 12 plaque psoriasis, three
non-lesional plaque psoriasis, five lesional eczema, and five nonlesional eczema samples were analyzed. In addition, one tonsil
sample from a guttate psoriasis patient affected by recurrent
streptococcal throat infections, two normal adult colon and one
fetal colon samples were used for immunohistochemistry. For
Western blot analysis, 10 normal, 12 plaque psoriasis, three nonlesional plaque psoriasis, seven guttate psoriasis, four non-lesional
guttate, five lesional eczema, and four non-lesional eczema samples
were considered.

Antibodies
The following antibodies were used: (1) Murine mAb L31 which
binds linear a1 domain epitope at position 67 of human HLA-C
alleles Cw1 through Cw8 and HLA-B8 and B51 (Setini et al., 1996).
Alleles from Cw9 to Cw17, and B8 and B51 do not associate with
psoriasis, therefore, under-or overestimation of expression levels is
expected to cancel out between patients and controls. (2) Murine
mAb W6/32 (Serotec, Oxford, UK) (Brodsky et al., 1979) which
binds MHC class I heavy chain associated with b-2-microglobulin.
(3) Murine mAb MCA2243 (NKVFS1) (Serotec) (Spaggiari et al.,
2002) which recognizes a common epitope on CD158a and
CD158b (KIR2DL1, KIR2DL2), and (4) horse radish peroxidaseconjugated rabbit polyclonal P0174 (DakoCytomation, Glostrup,
Denmark) which binds human b2m. As secondary antibody, horse
radish peroxidase-conjugated goat anti-mouse IgG (Santa Cruz,
sc-2005) was used.

Sample preparation
Skin biopsies were prepared as described previously (Carlen et al.,
2005). In brief, the biopsies were kept frozen in liquid nitrogen and
mechanically homogenized using a mortar and pestle. The samples
were then solubilized in a buffer containing 7 M urea, 2 M thiourea,
4% SDS, reducing agents, and protease inhibitors. Protein concentration was determined using the Bradford method (BioRad Protein
Assay, BioRad, Stockholm, Sweden) (Bradford, 1976).

Western blot
Total protein extracts were separated, adding 7 mg of each sample to
12% SDS-PAGE gels, and then electroblotted onto nitrocellulose
membranes (Whatman Schleicher & Schuell, Kent, UK). The
membranes were then stained with 1% Ponceau S (Sigma, St Louis,
MO) and scanned to check for loading and gel run quality. After
blocking with 2% goat serum (Vector Laboratories, Burlingame, CA)
and 1% BSA (Sigma, St Louis, MO) in Tris-buffered saline for 1 hour,
the membranes were incubated separately overnight with L31, W6/
32, MCA2243, or b2m antibody diluted 1:500 in TBS with 1%
Tween 20. The membranes were then incubated with horse radish
346

Journal of Investigative Dermatology (2007), Volume 127

peroxidase-conjugated goat anti-mouse IgG (Santa Cruz Biotechnology, Santa Cruz, CA) (except for b2m) diluted 1:2,000 in blocking
buffer followed by development using enhanced chemiluminescence (Amersham Pharmacia Biotech, Sunnyvale, CA) and the
image acquired with a CCD camera (Fujifilm, Sendai, Japan). The
immunoreactivity of the HLA-C and b2m antibodies was tested
against recombinant HLA-C and b2-microglobulin. Unspecific
binding of the secondary antibody was prevented by pre-incubation
in normal goat serum.

Immunohistochemistry
All biopsies were snap-frozen and stored at 701C until further
processed. Skin samples from lesional and non-lesional eczema and
plaque and guttate psoriasis, and healthy skin were included in the
same experiments. In short, 67-mm thick cryostat sections were
incubated with L31, W6/32, and MCA2243 antibody at 1:200,
1:20,000, and 1:200 dilutions, respectively. All sections were
stained using the avidin: biotinylated enzyme complex technique
(Vector Laboratories, Burlingame, CA) following the manufacturers
instructions, and counterstained with Gills III hematoxylin solution.
As controls, tissue sections were processed in parallel without
adding primary antibody. No reactivity for secondary antibodies or
signal developing reagents was observed on control histological
sections.

Cell culture
LCL721.221 cells were maintained in DMEM (Gibco-BRL Life
Technologies, Paisley, UK) supplemented with 10% FCS (fetal calf
serum; Hy-Clone, Boule Nordic AB Huddinge, Sweden) and
antibiotics (PEST _ penicillin 50 U/l and streptomycin 50 mg/ml;
Gibco-BRL) at 5% CO2 at 371C. HLA-Cw3 and Cw4 transfectants
were kept under G418 (GibcoBRL) selection. During stimulation
experiments, about 105 cells/well were grown in 12-well plates
without selection with G418 for 2 days and then exposed to 1 mg/ml
E. coli-derived lipopolysaccharide. HLA-C expression was detected
with the L31 antibody at time 0 and 16, 48 and 96 hours after
stimulation. The cells were then transferred to slides, fixed with
ethanol, and further processed as described in the immunohistochemistry section above.

Data analysis
Image analysis was carried out using Science Lab 99 L Process
software, version 1.95 (Fujifilm, Sendai, Japan). Intensity measurements of specific signals were corrected by the total amount of
protein in their corresponding lanes as derived from measurement of
Ponceau staining intensities of the membranes. Variations in
luminosity between images were adjusted by using an HLA-Cpositive cell line as internal control on every membrane and
the density values were adjusted using the following formulae:
Expression Index (corrected sample reading)/(corrected Ponceau
reading).
Corrected sample reading (sample density  (Strongest intergel
control/samples gel control))
Corrected Ponceau reading reading of control lane/sum of
readings from all lanes in gel
Statistical analysis was performed using the R language and
statistics package (Ihaka and Gentleman, 1996). Mean expression
indexes from different sample groups were compared by fitting a

L Carlen et al.
HLA-C Expression Pattern in Psoriasis

one-way analysis of variance model to the data, assuming a

significance level of 0.05. Then a paired t-test was performed in
order to identify comparisons with significant differences.
CONFLICT OF INTEREST
The authors state no conflict of interest.

ACKNOWLEDGMENTS
We thank Dr Eniko Sonkoly for critically reviewing this manuscript, AnnaLena Kastman for skilful technical assistance with immunohistochemistry,
Dr Gunther Weber for providing HLA-C-positive cell lines and for assistance
with immunoblotting, Dr Alberto Beretta for providing us with the L31
HLA-C antibody, Dr Jack Strominger, and Dr Hugh Reyburn for providing
HLA-C constructs, and Dr Kalle Malmberg and Dr Hans Gustav Ljunggren for
HLA-C transfected LCLs. This study was supported by funds from the
Swedish Research Council, the Swedish Heart and Lung Foundation, the
Swedish Psoriasis Association, Ake-Wibergs foundation, Serono, Biogen,
Schering-Plough, the National Psoriasis Foundation, Karolinska University
Hospital, and Karolinska Institutet.

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Journal of Investigative Dermatology (2007), Volume 127