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PubMed2000

Association and linkage of atopic dermatitis with chromosome 13q12-14 and 5q31-33 markers.

Atopic dermatitis is a chronic inflammatory skin disease that affects 10-20% of the population. Linkage of atopy, asthma, allergic rhinitis, and total serum IgE levels to several different chromosomal regions have been described extensively, but little is known about the genetic control of atopic dermatitis. We tested for the association and linkage between atopic dermatitis and five chromosomal regions: 5q31-33, 6p21.3, 12q15-24.1, 13q12-31, and 14q11.2/14q32.1-32.3. Marker analysis was performed in two Caucasian populations: (i) 192 unrelated German children with atopic dermatitis and 59 non-atopic children from a German birth cohort study (MAS'90), parental DNA was tested in 77 of 192 children with atopic dermatitis; (ii) 40 Swedish families with at least one family member with atopic dermatitis selected from the International Study of Asthma and Allergy in Children. Evidence for linkage and allelic association for atopic dermatitis was observed for markers on chromosome 13q12-14 and 5q31-33.

Child↗
PubMed2000

A Th2 chemokine, TARC, produced by keratinocytes may recruit CLA+CCR4+ lymphocytes into lesional atopic dermatitis skin.

Atopic dermatitis is an inflammatory skin disease in which the inflammation is characterized by the influx of lymphocytes into the dermis. It is generally believed that atopic dermatitis is a Th2-type disease, i.e., the T lymphocytes produce interleukin-4, interleukin-5, interleukin-10, and interleukin-13, although it has become evident in recent years that the cytokine profile in the skin changes during the course of the disease towards a Th1-Th2 mixed cytokine profile (interferon-gamma, tumor necrosis factor alpha, and interleukin-2). The lymphocytes that home into the skin express cutaneous lymphocyte-associated antigen, and it has recently been shown that most of the lymphocytes in this population express the chemokine receptor CCR4. CCR4 is the receptor for the CC chemokine TARC (thymus and activation regulated chemokine), and this chemokine is expressed predominantly by keratinocytes in the basal layer of the epidermis of lesional atopic dermatitis skin in mice. In humans, however, it was shown to be expressed in the endothelial cells of the dermis. We have examined the peripheral blood mononuclear cells of atopic dermatitis patients for the expression of cutaneous lymphocyte-associated antigen and CCR4 and compared them with peripheral blood mononuclear cells from normal controls. We found that the proportion of CLA+CCR4+ lymphocytes is upregulated in atopic dermatitis patients. In addition we have examined skin biopsies of lesional and non-lesional skin from atopic dermatitis patients and found that the keratinocytes, but not the endothelial cells, produce TARC in the lesional but not in the nonlesional skin. To gain insight in the stimulatory mechanisms for TARC production in keratinocytes, as previously observed in mice, we cultured HaCaT cells and found that interferon-gamma and tumor necrosis factor alpha work synergistically to induce TARC production. These observations suggest that the induction of TARC production in keratinocytes plays an important role in the late phase skin invasion by CCR4+CLA+ Th2-type lymphocytes in atopic dermatitis.

Animals↗
PubMed2000

Dysregulated activation of activator protein 1 in keratinocytes of atopic dermatitis patients with enhanced expression of granulocyte/macrophage-colony stimulating factor.

Keratinocytes of patients with atopic dermatitis produce high amounts of granulocyte/macrophage colony-stimulating factor, a factor essential for dendritic cell function and thus for the development of skin immune responses. In contrast to keratinocytes cultured from nonatopic, healthy individuals, granulocyte/macrophage colony-stimulating factor mRNA could be detected in unstimulated cultures of atopic dermatitis keratinocytes, and phorbol myristate acetate induced much greater granulocyte/macrophage colony-stimulating factor mRNA levels in these cells, although the decay kinetics were not altered. Using reporter gene (chloramphenicol acetyl transferase) analysis, a minimal granulocyte/macrophage colony-stimulating factor promoter was shown to confer constitutive and phorbol-myristate-acetate-induced regulation of transcriptional activity in keratinocytes, and significantly higher levels of chloramphenicol acetyl transferase activity were measured in lysates of unstimulated and phorbol-myristate-acetate-treated atopic dermatitis keratinocytes than in control keratinocyte cultures. Electrophoretic mobility shift assays showed that low levels of NF-kappa B binding activity could be induced by phorbol myristate acetate in both normal and atopic dermatitis keratinocytes. By contrast, activator protein 1 complexes were efficiently induced, and they were invariably present at higher levels in nuclear lysates of atopic dermatitis keratinocytes. Atopic dermatitis keratinocyte nuclear lysates had higher constitutive levels of c-Jun, and phorbol myristate acetate promoted an earlier and stronger expression of c-Jun, JunB, and of the phosphorylated forms of c-Fos. A dysregulated activation of activator protein 1 may be implicated in the molecular mechanisms leading to increased granulocyte/macrophage colony-stimulating factor expression in atopic dermatitis keratinocytes. J Invest Dermatol 115:1134-1143 2000

Adolescent↗
PubMed2001

Intracellular 3',5'-adenosine cyclic monophosphate level regulates house dust mite-induced interleukin-13 production by T cells from mite-sensitive patients with atopic dermatitis.

We studied the relationship between cAMP and house dust mite-induced cytokine production in T cells from mite-sensitive patients with atopic dermatitis. T cells from atopic dermatitis patients secreted high level of interleukin-13 (mean 851.1 pg per ml) when cultured with autologous monocytes pulsed with Dermatophagoides pteronyssinus extract. Dermato- phagoides pteronyssinus-induced interleukin-13 secretion was not detected in normal subjects. Adenylate cyclase inhibitor MDL 12,330A and cyclic nucleotide phosphodiesterase type 4 inhibitor rolipram blocked Dermatophagoides pteronyssinus-induced interleukin-13 secretion in atopic dermatitis T cells. In atopic dermatitis T cells, cAMP level rose at 5 min after Dermatophagoides pteronyssinus stimulus then decreased to the basal level at 1 h. MDL 12,330A blocked the Dermatophagoides pteronyssinus-induced cAMP elevation while rolipram blocked its reversal. In atopic dermatitis T cells, adenylate cyclase activity increased at 5 min after Dermatophagoides pteronyssinus stimulus, followed by the increase of cyclic nucleotide phosphodiesterase activity at 15 min. In atopic dermatitis T cells, phospholipase C inhibitor ET-18-OCH3 blocked Dermatophagoides pteronyssinus-induced activation of adenylate cyclase, while rolipram, protein kinase A inhibitor H-89, and MDL 12,330A blocked the activation of cyclic nucleotide phosphodiesterase. These results suggest that Dermatophagoides pteronyssinus may first increase cAMP in atopic dermatitis T cells by activating adenylate cyclase via phospholipase C, and next decrease cAMP by activating cyclic nucleotide phosphodiesterase 4 via protein kinase A, which may be activated by adenylate cyclase-generated cAMP signal. These events are required for interleukin-13 response Dermatophagoides pteronyssinus.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

Intradermal administration of a killed Mycobacterium vaccae suspension (SRL 172) is associated with improvement in atopic dermatitis in children with moderate-to-severe disease.

BACKGROUND: Although a doubling in the prevalence of atopic disease, including atopic dermatitis, in the Western world over the last few generations has been paralleled by a marked reduction in infectious diseases, especially tuberculosis, it is unclear whether this increase in atopy is causally related to reduced exposure to mycobacteria. OBJECTIVES: The aim of this study was to determine whether administration of mycobacterial antigens to atopic individuals might ameliorate their disease. METHODS: Forty-one children aged 5 to 18 years with moderate-to-severe atopic dermatitis were enrolled in a randomized, double-blind, placebo-controlled trial, where they were given either one intradermal injection of killed Mycobacterium vaccae (SRL 172) or buffer solution (placebo). Changes in skin surface area affected by dermatitis and dermatitis severity score were assessed before treatment and at 1 and 3 months after treatment. RESULTS: Children treated with SRL 172 showed a mean 48% (95% CI, 32%-65%) reduction in surface area affected by dermatitis compared with a mean 4% (95% CI, -29% to 22%) reduction for the placebo group (P <.001) and a median 68% (interquartile range, 46%-85%) reduction in dermatitis severity score compared with 18% (interquartile range, -2% to 34%) for the placebo group (P <.01) at 3 months after treatment. There were no untoward effects of the treatment, apart from a local reaction in 13 of the 21 children, which occurred 1 month after SRL 172 administration and settled spontaneously. CONCLUSION: SRL 172 was associated with an improvement in the severity of the dermatitis in children with moderate-to-severe disease.

Adolescent↗
PubMed2000

The association of atopic dermatitis in infancy with immunoglobulin E food sensitization.

OBJECTIVE: To prospectively investigate the association of high levels of immunoglobulin E (IgE) sensitization to foods and the presence of atopic dermatitis (judged by reported topical steroid use during the first 16 months of life) in a birth cohort of 620 Australian children "at risk" of allergic disease because of family history. RESULTS: A total of 559 of the children in the cohort were fully evaluated, and the cumulative prevalence of atopic dermatitis was 24%. More children in the cohort who had atopic dermatitis had strongly positive skin test results (> or = 4+, histamine equivalent units, > or = approximately 6-mm wheal), consistent with IgE food sensitization to either cow's milk, egg, or peanut at 6 months (22% vs 5%, chi(2) = 35; P < 10(-6)) and at 12 months (36% vs 11%, chi(2) = 41; P < 10(-6)) than those without atopic dermatitis. The calculated attributable risk percent for IgE food sensitization as a cause of atopic dermatitis was 65% and 64% at these times. In a separate group of infants with severe atopic dermatitis, the equivalent rates of IgE food sensitization at 6 months was 83% and at 12 months, 65%. CONCLUSION: IgE food sensitization is a major risk factor for the presence of atopic dermatitis in infancy.

Dermatitis, Atopic↗
PubMed2002

Atopic dermatitis and concomitant disease patterns in children up to two years of age.

There are few prospective studies of atopic dermatitis and co-existing diseases such as respiratory infections in children up to 2 years of age. Using annual questionnaires, we studied the cumulative incidence of atopic dermatitis and concomitant symptoms indicating other atopic diseases and respiratory infections in 0-2-year-old children in a prospective birth cohort of 4089 children. We found associations between atopic dermatitis and asthma (ratio of proportion 1.45, 95% CI 1.16-1.80), allergic rhinoconjunctivitis (RP 2.25, CI 1.77-2.85), adverse reactions to foods (RP 3.20, CI 2.83-3.62), urticaria (RP 2.04, CI 1.80-2.31), acute otitis media (RP 1.13, CI 1.05-1.21), more than one pneumonia during the first and/or second year of life (RP 2.17, CI 1.14-4.15), and use of antibiotics at least twice yearly (RP 1.29, CI 1.07-1.56). The association between atopic dermatitis and respiratory infections persisted after stratification for asthma. There was a higher proportion of atopic disease manifestations, but not respiratory infections, in children with onset of atopic dermatitis during the first year of life than during the second. The study shows that during the first 2 years of life there is a significant association not only between atopic dermatitis and other atopic disease manifestations, but also between atopic dermatitis and respiratory infections manifested in an increased rate of acute otitis media, pneumonia and use of antibiotics.

Acute Disease↗
PubMed2003

Atopic dermatitis in young children: diagnostic criteria for use in epidemiological studies based on telephone interviews.

The aim of the study was to establish diagnostic criteria for atopic dermatitis in 1.5-year-old children that could be employed in epidemiological studies of atopic dermatitis based on telephone interviews. In a Danish cohort of 100,000 pregnant women, 4 computer-assisted telephone interviews were carried out. In the last interview, conducted when the child was 1.5 years old, mothers were asked about their child's skin condition. Eighty-one women who had answered that their child suffered from either an itchy rash or atopic dermatitis were invited to participate in the study. Of these, 60 took part in the study and had their child examined by a dermatologist. Affirmative answers to 1) itchy rash or doctor-verified atopic dermatitis and 2) recurrent rash or rash for at least 4 consecutive 0.5-month periods, and 3) localization in elbow creases, behind the knees, wrists/hands, face or generalized rash resulted in the highest sensitivity and specificity for atopic dermatitis as diagnosed by the dermatologist, who found 37 of 60 children (62%) suffering from atopic dermatitis. Using this algorithm, telephone interviews can be used to diagnose atopic dermatitis in young children in large-scale epidemiological investigations.

Adult↗
PubMed2005

Thymus is enlarged in children with current atopic dermatitis. A cross-sectional study.

Atopic dermatitis is a common skin disorder of unknown aetiology with peak incidence in early childhood. The disease is associated with peripheral T-cell accumulation in the skin. The thymus is a key organ of the cellular immune response early in life. We hypothesized that atopic dermatitis is associated with an unbalanced establishment of the peripheral T-lymphocyte system. This cross-sectional study was performed to compare thymus sizes in patients with atopic dermatitis and healthy controls. Thirty-seven children with current atopic dermatitis were enrolled and compared with 29 healthy controls. An interview and medical examination were performed by one doctor, an ultrasound scan was performed within 3 days of the examination, and the thymus index, a marker of thymus size, was measured. The thymus index was on average 32% higher (95% CI 3%-67%) in children with active atopic dermatitis compared with healthy controls. It declined with age in both children with atopic dermatitis and healthy controls, but the reduction in size was only significant for healthy controls. We demonstrate increased size of thymus among children with active atopic dermatitis compared with healthy controls. The larger size of thymus is compatible with increased thymic activity and emission of T lymphocytes.

Case-Control Studies↗
PubMed1998

Expression of T cell receptor V beta chain in lesional skin of atopic dermatitis.

Atopic dermatitis is a chronic, relapsing inflammatory skin disorder characterized by local infiltration of T cells. To date, numerous reports have shown that Staphylococcus aureus may exacerbate atopic dermatitis, and superantigens produced by this organism are thought to be one of the major causative factors in atopic dermatitis. The purpose of this study was to evaluate the role of staphylococcal superantigen in atopic dermatitis by observing expression of the variable region of beta chain of T cell receptor (TCR V beta) in the inflammatory cells infiltrating cutaneous lesions of atopic dermatitis. Fourteen patients with atopic dermatitis were enrolled. Punch biopsy specimens were obtained from lesional and normal-appearing skin of all patients. The expression of TCR V beta was studied by means of immunohistochemical technique using monoclonal antibodies. In 4 out of 14 patients, the tendencies of preferential expression of specific TCR V beta were found in lesional skin. This study suggested that staphylococcal superantigen and its corresponding T cell subsets may act as causative or pathogenic factors in a subgroup of atopic dermatitis.

Adolescent↗
PubMed1998

The significance of previous contact dermatitis for elicitation of contact allergy to nickel.

In 2 earlier studies, we found increased nickel re-test reactivity at earlier experimentally induced nickel eczema sites. The aim of this study was to investigate if earlier contact dermatitis caused by another allergen or earlier irritant contact dermatitis also influenced the reactivity when nickel was applied topically on earlier but healed dermatitis sites. Twenty-three females with contact allergy to both nickel and cobalt were involved in the study. Experimental contact dermatitis from nickel, cobalt and SLS was induced on the lower back. One month later, challenge patch testing with a serial dilution of nickel on the previous but healed dermatitis sites, and on a control area, was done. The tests were read blindly. Significantly higher test reactivity was found at the site with previous allergic contact dermatitis from nickel, and significantly lower test reactivity was observed at the previous SLS dermatitis site.

Adult↗
PubMed2003

Gamma-linolenic acid supplementation for prophylaxis of atopic dermatitis--a randomized controlled trial in infants at high familial risk.

BACKGROUND: Studies suggest that low concentrations of n-6 long-chain polyenes in early life are correlated to atopic disease in later life. OBJECTIVE: The purpose of the study was to investigate the possible preventive effect of gamma-linolenic acid (GLA) supplementation on the development of atopic dermatitis in infants at risk. DESIGN: In a double-blind, randomized, placebo-controlled trial, formula-fed infants (n = 118) with a maternal history of atopic disease received borage oil supplement (containing 100 mg GLA) or sunflower oil supplement as a placebo daily for the first 6 mo of life. Main outcome measures were the incidence of atopic dermatitis in the first year of life (by UK Working Party criteria), the severity of atopic dermatitis (SCORing Atopic Dermatitis; SCORAD), and the total serum immunoglobulin E (IgE) concentration at the age of 1 y. RESULTS: The intention-to-treat analysis showed a favorable trend for severity of atopic dermatitis associated with GLA supplementation ( x+/- SD SCORAD: 6.32 +/- 5.32) in the GLA-supplemented group as compared with 8.28 +/- 6.54 in the placebo group (P = 0.09; P = 0.06 after adjustment for total serum IgE at baseline, age 1 wk), but no significant effects on the other atopic outcomes. The increase in GLA concentrations in plasma phospholipids between baseline and 3 mo was negatively associated with the severity of atopic dermatitis at 1 y (Spearman's correlation coefficient = -0.233, P = 0.013). There was no significant effect on total serum IgE concentration. CONCLUSION: Early supplementation with GLA in children at high familial risk does not prevent the expression of atopy as reflected by total serum IgE, but it tends to alleviate the severity of atopic dermatitis in later infancy in these children.

Dermatitis, Atopic↗
PubMed2000

Occupational contact dermatitis in the UK: a surveillance report from EPIDERM and OPRA.

Since February 1993 the EPIDERM surveillance scheme has collected data on occupational skin disease from consultant dermatologists in the UK. Reporting by occupational physicians to the scheme began in May 1994 and was superseded in January 1996 by the Occupational Physicians Reporting Activity (OPRA). The schemes currently receive reports on incident cases from 244 dermatologists and 790 occupational physicians. An estimated total of 9937 cases of contact dermatitis reported by dermatologists was calculated from surveillance data; 8129 contact dermatitis cases were estimated from reports by occupational physicians. The annual incidence of occupational contact dermatitis from dermatologist reports was 6.4 cases per 100,000 workers and 6.5 per 100,000 from reports by occupational physicians, an overall rate of 12.9 cases per 100,000 workers. Manufacturing industries account for the greatest number of cases seen by both sets of reporting physicians, with health care employment second. Reports from dermatologists also indicate high rates of dermatitis in the personal service industries (mainly hairdressers and barbers) and in agriculture. With the exception of an increase in cases seen in nurses in both schemes, the numbers and proportions of cases of contact dermatitis within occupations have remained fairly constant over the 6-year reporting period. Agents accounting for the highest number of allergic contact dermatitis cases were rubber (23.4% of allergic cases reported by dermatologists), nickel (18.2), epoxies and other resins (15.6), aromatic amines (8.6), chromium and chromates (8.1), fragrances and cosmetics (8.0), and preservatives (7.3). Soaps (22.0% of cases), wet work (19.8), petroleum products (8.7), solvents (8.0), and cutting oils and coolants (7.8) were the most frequently cited agents in cases of irritant dermatitis. The national scope of the data, together with the parallel structure by which both dermatologists and occupational physicians report incident cases, is useful in determining the extent of skin hazards in UK industry and may help in better targeting efforts to reduce the burden of skin disease at work.

Dermatitis, Occupational↗
PubMed1983

Histology of linear IgA disease, dermatitis herpetiformis, and bullous pemphigoid.

The histologic appearances of cutaneous biopsy specimens from 30 patients with linear IgA disease with a continuous band of IgA along the basement membrane, four patients with a linear pattern of granular IgA along the basement membrane, 26 patients with dermatitis herpetiformis who had IgA in the papillary dermis, and 23 patients with bullous pemphigoid who had IgG and/or C3 along the basement membrane were compared. Those with linear and granular IgA and dermatitis herpetiformis differed from those with bullous pemphigoid in five respects. Multiple microabscesses and fibrin at tips of papillae and leukocytoclasis were less common in bullous pemphigoid, whereas a dense infiltrate of eosinophils in and below bullae and a linear infiltrate of eosinophils along the basement membrane were more common in bullous pemphigoid. Also, multilocular bullae and acantholysis were more common in dermatitis herpetiformis than in bullous pemphigoid. Linear IgA disease differed from dermatitis herpetiformis in two respects. Acantholysis and fibrin at the tips of papillae and leukocytoclasis were more common in dermatitis herpetiformis. The specimens from patients with granular IgA did not differ significantly from those with linear IgA or dermatitis herpetiformis. The appearances of biopsy specimens of patch tests with potassium iodide taken from 11 patients with dermatitis herpetiformis and linear or granular IgA disease were similar to those taken from spontaneous lesions.

Adult↗
PubMed1994

Cashew nut dermatitis.

The urushiol dermatitis caused by plants of the Anacardiaceae family is the most common cause of acute allergic contact dermatitis. We have reported a case of cashew nut urushiol dermatitis due to ingestion of homemade cashew nut butter contaminated by cashew nut shell oil. With the precautions taken today to avoid contamination of food products with cashew urushiols, it is rare to find a case of cashew nut dermatitis in the United States. We have found no other report of contact dermatitis due to cashew nut butter. Moreover, though hinted at in the literature, there has been no previous detailed report of perianal contact dermatitis due to cashew ingestion. The fact that our patient was ill enough to require treatment with 3 weeks of systemic steroid therapy highlights the potential public health hazard of consumption of improperly prepared cashew products. However, the risk of cashew nut dermatitis today remains small, and this should not discourage cashew lovers from enjoying their treats. A final lesson to be learned from this case is that perianal eruptions may be due to materials deliberately applied to the anogenital region or to ingested antigens that remain sufficiently intact within the feces to affect perianal skin.

Acute Disease↗
PubMed1998

Hand dermatitis in intensive care units.

An investigation of the prevalence of occupational hand dermatitis in two intensive care units at a large teaching hospital was conducted. Information concerning the presence of occupational hand dermatitis, frequency of hand-washing, severity of the rash, aggravating conditions, history of atopy, and demographic factors (age, race, gender, and occupation) was collected via a self-administered questionnaire. The prevalence of occupational hand dermatitis was found to be 55.6% in the total reporting population of the units and was 69.7% in the most highly exposed workers (those reporting a frequency of hand-washing exceeding 35 times per shift). No relationship was found between occupational hand dermatitis and reported age, gender, race, atopic status, history of previous hand dermatitis, and duration of employment. Hand-washing frequency greater than 35 times per shift was strongly associated with occupational hand dermatitis (odds ratio = 4.13, P < 0.005). The high prevalence of occupational hand dermatitis found in this study of intensive care unit workers causes concern regarding the risk of health care workers in such units when exposed to blood-borne diseases.

Adult↗
PubMed1993

Increased interleukin 6 production by T cells derived from patients with atopic dermatitis.

Many immunologic aspects of atopic dermatitis have been studied, but basic pathobiologic mechanisms of this disease remain unknown. In this study, we measured the production of interleukin-6 (IL-6) by peripheral blood T cells and monocytes from patients with atopic dermatitis in comparison to normal control subjects and patients with chronic psoriasis. We found that peripheral blood T cells isolated from patients with atopic dermatitis produced significantly higher levels of IL-6 (36.1 +/- 5.1 units/ml, n = 22) than T cells derived from either normal subjects (12.6 +/- 1.9 units/ml, n = 22) or patients with chronic psoriasis (26.7 +/- 4.1 units/ml, n = 7). T-cell activation was also measured in the patients with atopic dermatitis by soluble serum IL-2 receptor levels and were found to be significantly higher (623.7 +/- 8.1 units/ml, n = 8) than normal subjects (357.2 +/- 26.0 units/ml, n = 8). In contrast to the increased production of IL-6 by T cells in atopic dermatitis, there was no significant difference in the IL-6 production by peripheral blood monocytes derived from patients with atopic dermatitis compared to normal subjects. Thus, peripheral blood T cells derived from patients with AD spontaneously produce increased amounts of IL-6 compared to T cells from normal subjects, which may reflect the increased activation state of T cells in atopic dermatitis. These data support the concept that activated T cells or subsets of T cells may be important effector cells in mediating inflammatory activity in atopic disease.

Biological Availability↗
PubMed1991

Molecular analysis of HLA DP and DQ genes associated with dermatitis herpetiformis.

HLA class II DQ and DP genes from dermatitis herpetiformis patients were amplified and analyzed using molecular probes and compared to those from celiac disease patients and to an HLA and ethnically matched control group. In dermatitis herpetiformis, as in celiac disease, the strongest association of disease was with the DQ subregion alleles DQB1*0201 and DQA1*0501 that are linked to the DRB1*0301 allele. DQB1*0201 determines the DQw2 serologic marker whereas DRB1*0301 determines the DRw17 serologic marker (formerly termed DR3). A DP subregion allele DPB1*0301 was increased and a constellation of DPB1 alleles that included DPB1*0202, *0901, and *1301 was decreased in dermatitis herpetiformis. DPB1*0101, an allele reported to be increased in celiac disease, was not increased in dermatitis herpetiformis. DP beta chains that lack a negatively charged amino acid residue at position 69 of the DP beta chain are significantly over-represented both in dermatitis herpetiformis and celiac disease patients with the DRw17, DQw2 haplotype, compared to healthy controls with that haplotype. These data favor a multigenic model for the contribution of HLA class II D region genes to dermatitis herpetiformis susceptibility. Further, they indicate that a specific DQ molecule, when present in combination with the product of one of several different DPB1 alleles, may contribute to susceptibility to the intestinal lesion, which is common to dermatitis herpetiformis and celiac disease.

Alleles↗