Dietary gluten challenge does not influence the levels of circulating immune complexes in patients with dermatitis herpetiformis

To examine the relationship between the gluten-sensitive enteropathy (GSE) and IgA circulating immune complexes (CIC) in dermatitis herpetiformis (DH) a series of dietary gluten-challenge studies were performed in patients with DH and patients with ordinary GSE. Serial serum samples were monitored for IgA-, IgG-, and IgM-containing CIC levels. In the first study, 9 DH patients and 5 controls were fed 20 g of gluten flour as a breakfast meal on 1 of 2 consecutive study days. DH patients did not develop or increase their levels of CIC after gluten-challenge or gluten-free meals. There was no significant difference between the DH patients and the control group in regard to development of CIC. To evaluate the effect of dietary gluten in another form, 8 DH patients were given meals containing 100 g of boiled Canadian cracked wheat. Two patients with ordinary GSE were also challenged with cracked wheat. Again there was no elevation or induction of CIC above baseline determinations by gluten-challenge meals. These studies suggest that dietary gluten does not induce the formation of CIC in patients with DH.     

Circulating antibodies to gliadin subfractions in dermatitis herpetiformis and linear IgA dermatosis of adults and children

Dermatitis herpetiformis (DH) and coeliac disease (CD) are linked but their association with linear IgA dermatosis (LAD) is unclear. Thirty-seven patients with DH and 27 with linear IgA dermatosis were investigated, of which 23/37 DH patients and 1/10 LAD patients had small intestinal enteropathy. Elevated IgG and IgA gliadin antibodies were found in the DH patients with enteropathy (CD). IgG gliadin antibodies in DH patients were directed against alpha, beta, gamma and omega gliadin subfractions. Elevated IgA gliadin antibodies in the adult LAD patients (n= 14) suggests that this condition may be associated with enteropathy or an IgA diathesis.     

Circulating antibodies to gliadin subfractions in dermatitis herpetiformis and linear IgA dermatoses

Dermatitis herpetiformis (DH) and coeliac disease are associated and the rash of DH is gluten-dependent. The gliadin fraction responsible for the rash is unknown. In linear IgA dermatoses the role of gluten in the skin eruption remains controversial.
Anti-gliadin antibodies (AGA) were measured by an enzyme-linked immunosorbent assay in 10 normal controls; 35 patients with dermatitis herpetiformis (DH); 14 adults with linear IgA disease; and 13 patients with chronic bullous dermatosis of childhood. The presence of enteropathy was assessed by jejunal biopsy and intra-epithelial lymphocyte (IEL) counts.
DH with normal IEL counts on normal diet: IgG and IgA-AGA identical to controls. DH with raised IEL counts on gluten-free diet: slightly elevated IgG and IgA-AGA. DH with raised IEL counts on a normal diet: IgG and IgA were higher, with median IgG 1:2048 (control 1:512) median IgA 1:512 (control 1:128). DH patients with high IgG AGA had elevated titres to α, β, γ, and ω subfractions. The highest levels were for α and the lowest for ω.
For linear IgA disease IgG is normal but adults had raised IgA-AGA compared to controls ( P = 0.005).
In dermatitis herpetiformis the presence of anti-gliadin antibody was dependent on the degree of enteropathy, and, if present, was directed against all gliadin subfractions. The significance of the elevated IgA—AGA in the linear IgA disease is unknown.     

Frequency and isotype distribution of serum antibodies reactive with dietary proteins in adults with chronic urticaria

Forty-eight adult patients with chronic urticaria have been evaluated for scrum antibodies reactive with bovine milk, chicken ovalbumin or wheat gliadin using a solid-phase enzyme-linked immunosorbent assay (ELISA). Of the chronic urticaria sera, 60.4% contained detectable antibodies reactive with one or more of these dietary antigens, compared with 33.9% of sera from 232 healthy adults (P < 0.001). In particular, antibodies reactive with milk (52%; P < 0.001), ovalbumin (39.6%, P < 0.001) and gliadin (20.8%, P > 0.05) were detected at increased frequencies compared with controls (22.8%, 16.8% and 11.6%, respectively). These serum antibodies were predominantly of the IgG isotype, with an IgG subclass restriction mainly to IgG4 for anti-ovalbumin and anti-gliadin antibodies, and to IgG2 and IgG4 for anti-milk antibodies. The increased frequency of IgG antibodies was not significantly associated with either raised total serum IgE or atopic status.     

Sequential studies of gliadin antibodies in patients with dermatitis herpetiformis

Summary Sequential studies of circulating gliadin antibodies (IgG, IgA, IgM, IgD) were performed in 24 patients with dermatitis herpetiformis (DH) by an ELISA. Three groups of patients were studied: (a) 14 patients who responded to a gluten-free diet and were able to stop their drug therapy, (b) 5 patients who did not respond to a gluten-free diet, (c) 5 patients with normal jejunal biopsies, who did not receive a gluten-free diet. Most of the serum gliadin antibodies detected were of IgG class, but in several patients IgA gliadin antibodies were found in addition. When the patients were on a normal diet, 63% had elevated IgG gliadin antibody titres (titres which exceeded the maximum titre of the controls by one dilution) and there were no significant differences between the three groups. When the patients were followed up, there was a significant fall in the gliadin antibody titres in those who responded to a gluten-free diet compared to the two other groups of patients. Thus assays of IgG gliadin antibodies might be helpful in some patients in judging the complicance of patients on a gluten-free diet.     

IgA anti-endomysium antibody. A new immunological marker of dermatitis herpetiformis and coeliac disease

The recently described IgA anti-endomysial antibodies (IgA-EmA) are directed against the intermyofibril substance of the smooth muscle, which may correspond either to a reticulin-like structure or a surface component of smooth muscle fibrils. These antibodies occurred in about 80% of sera of thirty-eight patients with dermatitis herpetiformis (DH), in about 70% of twenty-eight patients with coeliac disease and in about 20% of nine patients with other enteropathies. IgG class anti-gliadin antibodies (AGA) also occur in each of these diseases. Both antibodies were detected on monkey oesophagus by immunofluorescence. The IgA-EmA could not be detected in 122 control sera from patients with other gut or skin diseases, including fifteen cases with ulcerative colitis and fifteen cases with linear IgA bullous dermatosis (LABD). The presence and the titre of IgA-EmA and AGA paralleled the severity of the jejunal changes in patients with coeliac disease.     

Soluble interleukin-2 receptor levels in patients with dermatitis herpetiformis

To determine the role of T-cell activation in dermatitis herpetiformis (DH), soluble IL-2R levels were measured by enzyme-linked immunosorbent assay (ELISA) in the sera of 30 patients with DH. Levels of this shed receptor are considered to be a measure of in vivo T-lymphocyte activation, and are elevated in the sera of many patients with inflammatory and immune-mediated diseases. Fifteen of the thirty (50%) patients with DH had elevated levels of soluble IL-2R compared to one of 31 (3%) healthy HLA-B8 or HLA-DR3 control subjects (p less than 0.00001) and one of 10 (10%) healthy non-HLA-B8/-DR3 subjects (p less than 0.0018). In addition, the mean soluble IL-2R level in the patients with DH (744 +/- 381 U/ml) was also significantly higher than that seen in 31 healthy HLA B8 or HLA DR3 individuals (388 +/- 160 U/ml, p = 0.0001) and 10 healthy non-HLA-B8/DR3 individuals (397 +/- 201 U/ml, p = 0.002). Only two of the 30 patients with DH had active skin lesions at the time of serum sampling, one of whom had elevated levels of IL-2R. Measurement of soluble IL-2R levels in sequential serum samples, available in four patients with DH at times of active and inactive skin disease, demonstrated a temporal association between soluble IL-2R level elevations and active skin disease in two patients and no association in two patients. In one patient a marked elevation in soluble IL-2R levels occurred with the onset of gastrointestinal symptoms, which decreased by 14% with institution of a gluten-free diet. In order to determine if soluble IL-2R levels are related to the mucosal immune response, the IL-2R levels were compared to the level of IgA antibodies directed against the dietary antigen beta-lactoglobulin. Ten of eleven (91%) patients with circulating IgA anti-beta lactoglobulin antibodies were also found to have elevated levels of IL-2R. In contrast, in the patients with no detectable IgA anti-beta lactoglobulin antibodies, only four of 16 (25%) had elevated levels of IL-2R (p = 0.001). Because IL-2R levels are not related to activity of the skin disease in patients with DH but are associated with the presence of IgA antibodies against the dietary antigen beta-lactoglobulin, these results suggest that some of the T-cell activation commonly present in DH reflects an ongoing immune response in the gastrointestinal tract.     

Increased gliadin antibodies in dermatitis herpetiformis and pemphigoid

The mean titres of serum IgG and IgA gliadin antibodies were significantly increased in thirty-four patients with bullous pemphigoid, and in twenty-three patients with dermatitis herpetiformis, compared with twenty-four healthy controls. The patients with pemphigoid also had increased IgG and IgA gliadin antibodies compared with nine patients with pemphigus. The reason for the high titres of gliadin antibodies in pemphigoid is obscure. These patients may have increased intestinal permeability (suggested by the presence of beta-lactoglobulin antibodies in some patients). Alternatively gliadin may somehow precipitate the autoimmune process.     

Alterations in HLA-DP and HLA-DQ antigen frequency in patients with dermatitis herpetiformis

Dermatitis herpetiformis (DH) is associated with a markedly increased frequency of the HLA class II antigens DR3 and DQw2. To investigate a possible role of HLA-DP (or closely associated genes) in the pathogenesis of DH as well as to confirm the previously described alterations of HLA-DR3 and HLA-DQw2 antigen frequency, we have typed 43 patients with DH for HLA-DP, HLA-DQ, and HLA-DR antigens. All patients with DH had typical clinical and histologic features, as well as granular deposits of IgA at the dermal-epidermal junction by direct immunofluorescence. HLA-DR3 was expressed in 41 of 43 (95%) DH patients, whereas HLA-DQw2 was expressed in all 43 (100%). The overall distribution of HLA-DP antigens in patients with DH was significantly different from that seen in all controls and in HLA-DR3 and HLA-DQw2 controls (p less than 0.02). Examination of the frequency of individual DP antigens revealed that HLA-DPw1 was increased (42% of patients with DH vs 11% of all controls and 26% of DR3 positive controls), but this increase was not statistically greater than that expected due to the disequilibrium linkage of DPw1 with DR3/DQw2. Patients with DH, however, did have a statistically significant decreased frequency of DPw2 (14% of patients vs 31% of all controls and 41% of DR3 positive controls) (pc less than 0.05). Studies of three informative families demonstrated that the DPw2 genes of the DH patients were not present on the haplotype thought to carry a DH susceptibility gene (HLA-A1, HLA-B8, HLA-DR3, HLA-DQw2). A role of HLA-DP region genes in the pathogenesis of DH is further suggested by the observation that HLA-DPw1 was expressed in 82% (9 of 11) of DH patients with IgA antibodies against dietary antigens as compared with only 33% (4 of 12) of patients without IgA antibodies. HLA-DP genes or genes closely linked to them may be important in DH either as markers of the disease haplotype or by direct involvement in its pathogenesis.     

Serologic markers of gluten-sensitive enteropathy in bullous diseases.

BACKGROUND AND DESIGN--Dermatitis herpetiformis (DH) is characterized immunologically by the presence of IgA immune deposits in the skin and by the presence of various serum antibodies. Of these, antibodies to gliadin, reticulin, and endomysium have been found to be significant. There are, however, conflicting reports as to the exact specificity and sensitivity of these serologic markers in diagnosing DH. We examined the disease specificity of these three antibody markers in 14 patients with DH, in 98 patients with pemphigus and pemphigoid, and in 26 normal subjects. Reticulin and endomysium antibodies were detected by indirect immunofluorescence and gliadin antibodies by means of the enzyme-linked immunosorbent assay method. RESULTS--Among the various bullous diseases, endomysial and reticulin antibodies were found to be disease specific for DH. Endomysial antibodies occurred in twice the number of DH patients (72%) compared with the occurrence of reticulin antibodies (36%). Antigliadin antibodies were detected in two thirds of DH patients and were not disease specific since increased frequencies of these antibodies were also detected in patients with pemphigus and pemphigoid. CONCLUSION--These studies support the earlier findings of the high degree of specificity of endomysial antibodies for DH and, thus, help to differentiate DH from other bullous disorders.     

Wheat protein antibodies in dermatitis herpetiformis

An enzyme-linked immunosorbent assay was used to detect class-specific antibodies to wheat protein antigens. Antibodies which we detected by this technique reacted indistinguishably with antigens prepared from crude gluten, crude gliadin, alpha-gliadin, Frazer fraction III, and subfraction B and B3 of Frazer fraction III. No sera reacted with a human serum albumin control antigen. The prevalence of IgG antibodies to wheat protein antigens was significantly greater in patients with gluten sensitive enteropathy, 12 of 17, (p = .00011) and in patients with dermatitis herpetiformis, 5 of 14, (p = .046) than in normal control subjects. Strongly positive reactions for IgG antibodies were present only in patients with gluten sensitive enteropathy or dermatitis herpetiformis. IgA antibodies to wheat protein antigens were found only in gluten-sensitive enteropathy patients. We have found this to be a sensitive, precise technique for measurement of antibodies to wheat protein antigens and feel that it will prove useful in evaluation of the role of immune complexes involving wheat protein antigens and their antibodies in the pathogenesis of dermatitis herpetiformis.     

Serologic markers of celiac disease in psoriatic patients

Background  Aetiopathogenesis of psoriasis is complex and not yet well known. In recent years, it has been observed that psoriasis can coexist with clinically asymptomatic celiac disease and a gluten-free diet helps to obtain remission, even in patients with very chronic lesions.
Objective  The aim of our work was to investigate how often the positive titres of antibodies characteristic for celiac disease occur in psoriatics' serum in exacerbation in comparison with controls.
Patients/methods  Serum samples from 67 patients with intensified psoriatic lesions were investigated. Serum from healthy people at a comparable age and with no familial predisposition to psoriasis and celiac disease was the control material. Antibodies against human tissue transglutaminase (recombinant antigen), against tissue transglutaminase isolated from guinea pig's liver and against gliadin were determined by enzyme-linked immunosorbent assay technique. Anti-endomysial antibodies were determined by indirect immunofluorescence method.
Results  Patients with psoriasis have significantly higher mean concentrations of antibodies against tissue transglutaminase (human recombinant and guinea pig-derived antigen) and against gliadin for IgA. IgA antibodies against tissue transglutaminase (both antigens) and gliadin positively correlate with psoriasis activity. No anti-endomysial antibodies for IgA were found in any serum.
Conclusions  Our results seem to imply an association between psoriasis and asymptomatic celiac disease/gluten intolerance. High percentage of positive results to guinea pig-derived tTG could be due to cellular activity of tissue transglutaminase in psoriasis.     

Detection of antibodies to Neisseria gonorrhoeae in cervicovaginal secretion and in serum

In 33 female patients suffering from gonorrhoea, we searched for specific antibodies (IgA, IgG, IgM) directed against gonococci by means of the indirect immunofluorescence technique. This investigation was performed both before and after specific treatment. In comparison to 17 healthy women, we found increased rates of IgA and IgG antibodies in the secretion of our patients, the IgA rate being slightly higher than the IgG count; IgM was not detectable at all. In the serum, IgG antibodies clearly dominated over IgA and IgM. After successful treatment, IgA antibodies showed a more rapid reduction than IgG in both secretion and serum.     

Serum antibodies to wheat germ agglutinin and gluten in patients with dermatitis herpetiformis

Summary It has been speculated that gluten may play a role in the pathogenesis of dermatitis herpetiformis (DH) because it can act as a lectin. The lectin activity of gluten preparations was recently identified as wheat germ agglutinin (WGA). IgG and IgA serum antibodies to WGA and gluten were therefore measured in patients with DH and coeliac disease (CD) by an enzylac-linked immunosorbent assay (ELISA). Compared with healthy controls, both patients categories had increased IgG and IgA activities to WGA and gluten, the CD group showing the highest antibody levels. DH patients with subtotal villous atrophy tended to have higher activities than those with no villous changes or only minor changes. No significant difference in the gluten-to-WGA ratio of IgA or IgG antibodies was found when DH patients were compared with CD patients. If WGA plays a pathogenetic role in DH, then DH patients must have dermal characteristics, as yet undefined, that explain the initiation of their skin disease.     

Rheumatoid factor in sera of dermatitis herpetiformis patients

Serum specimens from 44 patients with dermatitis herpetiformis (DH) and 42 control patients were analyzed with solid-phase radioimmunoassay (RIA) developed to detect IgG and IgM class antibodies against herpes simplex virus (HSV) envelope antigen. They were also tested with different tests to detect rheumatoid factor (RF) as well as serum antibodies to gastric parietal cells, glomerular basement membrane, smooth muscle, mitochondria and nuclei. Total serum IgG, IgM and IgA quantification was performed concurrently. IgM class antibodies reacting in HSV envelope antigen RIA were found in 47.8% of the DH patients, but in none of the controls. The age distribution of the IgM positive patients was in accordance with the appearance of RF, representing elderly persons. The presence of RF in serum specimens was confirmed by removing the IgM reactivity with heat aggregated human gamma globulin adsorption and in 13 patients with positive serological tests for RF. No correlation was found with the appearance of RF and duration or severity of the disease or with the detection of RF and serum total IgM concentration. In DH patients antibodies to gastric parietal cells were found in 6 and to smooth muscle in 1 of 32 specimens tested.     

IgA immune complexes in patients with dermatitis herpetiformis occur in the absence of IgA rheumatoid factor

Thirty to forty percent of patients with dermatitis herpetiformis (DH) have IgA-containing circulating immune complexes (IgA-CIC); however, the antigenic composition of these complexes as well as the role they play in the pathogenesis of DH are unknown. The failure to detect wheat protein in these IgA-CIC, despite the association of DH with gluten-sensitive enteropathy, suggests that the IgA-CIC in DH may be similar to those seen in the IgA nephropathies and represent IgA rheumatoid factor (RF)-IgG complexes. We have examined the sera of 32 patients with DH, 16 non-DH patients positive for RF by latex fixation, and 15 normal subjects for IgA and IgM RF using enzyme-linked immunosorbent assays (ELISAs) and for IgA-CIC using an anti-C3 ELISA. Thirteen of 16 (81%) latex fixation test-positive patients had IgA RF by ELISA and 15/16 (94%) had IgM RF by ELISA. The total amount of RF detected by the ELISA (IgA + IgM RF) correlated with the latex fixation titer (r = 0.678, p = 0.004) in these latex fixation-positive patients. Six of the 16 (38%) latex fixation-positive patients also were found to have IgA-CIC. Solid phase absorption using goat antihuman C3 decreased the levels of immune complexes but not the level of IgA RF, suggesting the IgA-CIC detected do not represent uncomplexed IgA RF. In contrast, although 12 of 31 (39%) patients with DH had IgA-CIC ranging in amount from 0.331-26.0 micrograms IgA/ml (nl less than 0.150 microgram IgA/ml), only 1 of 32 (3%) DH patients had detectable levels of IgA RF (7.0 micrograms IgA/ml, nl less than 2.0 micrograms IgA/ml). Low levels of IgM RF were found in 8/32 (25%) of patients with DH (1.1-1.6 micrograms IgM/ml, nl less than 1.0 microgram IgM/ml). These data document that IgA RF is not present in the sera of patients with DH independent of the presence or absence of IgA-CIC and that it is unlikely that the IgA-CIC present are IgA RF complexed with autologous IgG.     

Circulating IgA- and IgG-class antigliadin antibodies in dermatitis herpetiformis detected by enzyme-linked immunosorbent assay

Summary A sensitive and technically simple enzymelinked immunosorbent assay (ELISA) was developed to demonstrate circulating IgA- and IgG-class antibodies to gliadin, a component of wheat gluten. Serum samples from 24 patients with dermatitis herpetiformis (DH), 5 with coeliac disease (CD) and 75 normal controls were analysed. Antigliadin antibodies (AGA) of the IgA class were detected in 71% of DH patients, all of the CD patients and 19% of the controls. IgG-AGA was found in over 90% of DH patients and controls and in all of the CD patients. The mean ELISA values of both IgA- and IgG-class AGA were significantly higher in DH patients than in the controls. The occurrence of circulating IgA-class AGA is compatible with the hypothesis that these antibodies can be deposited in the skin, e.g. as immune complexes, or due to cross-reactivity of gliadin and dermal reticulin.Supported by grants from the Foundation for Finnish Chemical Research     

Patients with psoriasis often have increased serum levels of IgA antibodies to gliadin

It was recently observed that in six patients with psoriasis and one with palmoplantar pustulosis. with newly discovered gluten intolerance, a gluten-free diet had a remarkable effect on the skin lesions. This prompted us to undertake a screening investigation to discover whether increased levels of serum antibodies to gliadin are more common in patients with psoriasis than in healthy persons. IgA and IgG antibodies to gliadin (IgA AGA and IgG AGA) were quantified by a micro-ELISA method. Out of 302 patients with psoriasis. 16% (18 females, 31 males) showed serum IgA AGA levels above the 90th percentile value (51 u/ml) of the reference group. This tendency was even more marked when the proportion of patients with values >70 u/ml was compared with the corresponding proportion of 99 reference subjects. Thus, 3% of the reference subjects but 7.9% of the patients had values >70 u/ml. The corresponding figures for men were 1.6% and 8.9%. respectively. Men with psoriasis had a significantly bigher mean IgA AGA than the male reference group. The means based on logarithmic values of the individual IgA AGA values were significantly higher in the psoriatic groups than in the reference groups. Although the mean level of IgG AGA was not increased in the psoriasis group, there was a correlation between the values for IgA AGA and IgG AGA. The serum concentrations of IgG, IgA and IgM were also measured. In the male patients, the mean IgA value was significantly increased. Women in whom IgA AGA was elevated also showed a significantly increased mean IgA. There was no correlation between the IgA AGA and the IgA values. The IgG levels were significantly elevated in both men and women with psoriasis, whereas the IgM levels did not differ from those in the reference group. Studies on the clinical relevance of the findings in this report, both with regard to the activity of the psoriasis and to the presence of intestinal abnormalities, are in progress.     

Dermatitis herpetiformis

The state of our understanding of the pathogenesis of DH relies on the integration of several key characteristics: (1) a high frequency of the HLA antigens HLA-B8, HLA-DR3, and HLA-DQw2, (2) an associated GSE, (3) the resolution of both the skin lesions and gut abnormalities in response to a gluten-free diet, and (4) the presence of granular deposits of IgA in normal and perilesional skin. The role of the HLA class II antigens expressed in patients with DH most likely relates to the afferent or initiating arm of the immune system. The association of the HLA-A1, -B8, -DR3, -DQw2 haplotype with Sjogren's syndrome, chronic hepatitis, Graves' disease, and other presumably immunologically mediated diseases, as well as the evidence that some normal HLA-B8, -DR3 individuals have an abnormal in vitro lymphocyte response to wheat protein and mitogens and have abnormal Fc-IgG receptor-mediated functions, suggests that this HLA haplotype or genes linked closely to it may confer a generalized state of immune susceptibility on its carrier, the exact phenotypic expression of which depends on other genetic or environmental determinants. It also is clear, from the association of DH with GSE and the ability to control the cutaneous manifestations of DH with a gluten-free diet, that the gut disease is a critical factor in the pathogenesis of DH. Several pathogenetic theories about the origin of the cutaneous IgA deposits in DH have been proposed, one of which states that the IgA is produced in the gut mucosa as a response to a dietary antigen or gut epithelial antigen and then cross-reacts with the skin of patients with DH. A second hypothesis is that the IgA produced in the gut binds to an antigen and is deposited in skin as an antigen-antibody complex. Finally, it could be that the gut mucosal abnormality simply allows an unknown antigen access to the central immune system where an IgA antibody is produced that binds to skin. The failure to detect circulating IgA anti-basement membrane zone antibodies in patients with DH suggests that either the structures to which the IgA binds are not present in normal skin without DH, that IgA cannot bind to these structures in vitro, or that the circulating IgA is too scant for detection with conventional methods. Finally, it must be considered that the IgA deposited in DH skin may bind as a result of non-antigen-antibody interactions that cannot be duplicated in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)     

Failure to detect specific gluten antigens associated with the immune aggregates in the skin in dermatitis herpetiformis

Summary The univolved skin of 10 patients with dermatitis herpetiformis (DH) was examined for the presence of gluten antigens with the immunofluorescence technique using a rabbit anti-gliadin antiserum, human antibodies to wheat and to reticulin conjugated to fluorescein-isothiocyanate (FITC) and class-specific anti-human lgA immunoglobulin.In all patients, IgA deposits were found in the tips of the dermal papillae of the uninvolved skin. With the anti-wheat and anti-reticulin conjugates, as well as with the rabbit anti-gliadin antiserum, no specific immunofluorescence was observed in any of the skin specimens. Skin biopsy sections of three DH patients were treated with an acid solution (pH 3.2) in an effort to dissociate antigen-antibody complexes that might be present. After the elution procedure the sections showed undiminished IgA fluorescence, and retesting with the anti-wheat- and antireticulin antisera again gave negative results. The skin eluates, two of which contained IgA, had no antibodies to wheat or reticulin.These findings do not give support to the hypothesis that the antigens in the suspected immune complexes in the DH skin consist of gluten.

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Zusammenfassung Die nicht angegriffene Haut von 10 Patienten mit Dermatitis Herpetiformis (DH) wurde auf die Anwesenheit von Gluten-Antigenen mit der Immunfluorescenztechnik untersucht unter Anwendung eines Antigliadin-Antiserums in einem Kaninchen erzeugt, menschliche Antikörper gegen Weizen sowie gegen Retikulin verbunden mit Fluorescein-Isothiocyanate (FITC) und mit spezifisch klassifiziertem anti-menschlichem IgA-Immunglobulin.In allen Patienten fanden sich IgA-Niederschläge in den Spitzen der Dermalpapillen der nicht angegriffenen Haut vor. Sowohl mit den Antiweizen- und Antiretikulinverbindungen als auch mit dem erwähnten Antigliadin Antiserum konnte keine spezifische Immunfluorescenz in den untersuchten Häuten festgestellt werden. Hautbiopt-Schnitten von 3 DH-Patienten wurden mit einer Säurenlösung (pH 3,2) erprobt, um zu versuchen, die Antigen-Antikörperverbindungen, die möglicherweise anwesend sein könnten, voneinander zu trennen. Nach der oben erwähnten Erprobung zeigten die Versuchsteile eine ungeänderte IgA-Fluorescenz, und nach Wiederholung der soeben genannten Probe mit Antiweizen- und Antiretikulin-Antikörper zeigten sich abermals negative Resultate.Die Hauteluaten, von denen zwei IgA enthielten, zeigten keine Antikörper gegen Weizen oder Retikulin. Diese Resultate tragen nicht zu der Hypothese bei, daß die Antigene in den vermutlichen Immunverbindungen in der DH-Haut aus Gluten bestehen.