Complementation with HLA-A and HLA-D locus alleles in ankylosing spondylitis with peripheral arthritis

Fifty-nine patients with HLA-B27 positive ankylosing spondylitis were HLA genotyped to look for immunogenetic differences between patients with associated peripheral arthritis and those with disease limited to the axial skeleton. An association was found between the peripheral arthropathy and 2 antigens, HLA-A11 and HLA-DR7 at the p less than 0.05 level. Complementation between these 2 alleles and HLA-B27 occurred in both the cis and trans positions. Four patients with peripheral arthritis had a rare HLA-B27 haplotype (HLA-B27, HLA-DR7) which was not found in the group with axial disease alone.     

HLA B27 and the genetics of ankylosing spondylitis.

One hundred and twenty-eight of 145 patients with ankylosing spondylitis (AS) were found to be HLA B27 positive. Five patients had evidence of a sero-negative peripheral arthritis resembling peripheral psoriatic arthritis and 3 of these were B27 negative. One further B27 negative patients had a sister with ankylosing spondylitis and ulcerative colitis and a mother with ulcerative colitis. There was evidence of a somewhat later age of onset of symptoms in B27 negative patients. These findings are interpreted as suggesting some degree of clinical and genetic heterogeneity in ankylosing spondylitis with genes for psoriasis and inflammatory bowel disease being important in some individuals, particularly those who are B27 negative. Twenty-five first-degree relatives with ankylosing spondylitis were all B27 positive. The only instance of disassociation of B27 and spondylitis in a family was where the proband had ulcerative colitis as well as spondylitis. Of 13 B27 positive fathers 3 could be diagnosed as having definite ankylosing spondylitis (23%). These findings are thought to provide evidence against the concept that the gene for ankylosing spondylitis is not B27 but a closely linked gene and favour the occurrence of an environmental event affecting approximately one-fifth of B27 positive males to result in disease.     

HLA-B27 in possible ankylosing spondylitis with peripheral arthritis

Summary Among 86 patients selected as possibly having ankylosing spondylitis because of clinical symptoms and radiologically normal sacroiliac joints, HLA-B27 was positive in 41%. Four years later a representative sample of 38 individuals were re-examined and radiographed. HLA-B27 positive patients developed sacroiliitis as defined by radiological criteria twice as often (P<0.05). They also showed increased uptake of technetium 99 m upon quantitative scintigraphy with a region of interest method and more often probable or definite ankylosing spondylitis as defined by the New York criteria. Further differences between the HLA-B27 positive and negative follow-up groups concerned the frequency of clinical symptoms and peripheral arthritis. It is suggested that HLA-B27 typing may be helpful both in diagnosis and in judging the prognosis of possible or abortive ankylosing spondylitis.     

Histocompatibility antigens in inflammatory bowel disease. Their clinical significance and their association with arthropathy with special reference to HLA-B27 (W27).

Histocompatibility (HLA) antigen phenotypes have been studied in 100 patients with ulcerative colitis, 100 with Crohn's disease, and 283 normal controls. In addition the incidence of ankylosing spondylitis, sacroiliitis, and "enteropathic" peripheral arthropathy was determined in the patients with inflammatory bowel disease (IBD). There was no significant difference in antigen frequency between patients and controls. However, the incidence of HLA-B27 was increased in the patients complicated by ankylosing spondylitis and/or sacroiliitis in both ulcerative colitis and Crohn's disease. In contrast, none of the 29 IBD patients with "enteropathic" peripheral arthropathy had B27 antigen. Furthermore, ankylosing spondylitis was found more frequently in ulcerative colitis bearing HLA-B27 compared with non-B27 patients (P less than 0-01). The same was found in Crohn's disease, although this difference was not statistically significant. In addition, 12 of 14 ulcerative colitis patients and five out of six Crohn's patients with HLA-B27 had total colitis, compared with the frequency of total colitis in non-B27 patients (P less than 0-024 and less than 0-03 respectively). The data suggest that B27 histocompatibility antigen could be a pathogenetic discriminator between the arthropathies in IBD and may be of prognostic significance with respect to extension and severity of the disease.     

Genetic differences between B27 positive patients with ankylosing spondylitis and B27 positive healthy controls

In a controlled study of the 499 available first degree relatives of 79 consecutive HLA-B27 positive patients with ankylosing spondylitis and 69 HLA-B27 positive healthy blood donors, 19 cases of ankylosing spondylitis were found: 16 (15 B27 positive) among the 282 relatives of the patients with ankylosing spondylitis, and 3 (1 B27 positive, 1 B27 negative, 1 unknown) among the 217 relatives of healthy donors (chi c2 = 5.11; P less than 0.025). However, if all cases of possible spondylarthritis are included, 48 cases of ankylosing spondylitis were found: 37 of 282 relatives of patients with ankylosing spondylitis and 11 of 217 relatives of healthy donors (chi c2 = 8.29; P less than 0.01). Assuming that 50% of relatives of B27 positive individuals carry this antigen, 15 of 142 (10.6%) B27 positive relatives of patients and 2 of 108 (1.9%) B27 positive relatives of healthy subjects (chi c2 = 5.91; P less than 0.025) have ankylosing spondylitis. The relative risk of spondylarthropathy for B27 positive relatives of B27 positive patients compared with relatives of B27 positive healthy subjects is 5.6. Assuming all subjects were evaluated in a similar manner, analysis of these data suggests genetic differences between B27 positive diseased individuals and B27 positive healthy subjects.     

Undifferentiated spondyloarthropathies in Brazilians: importance of HLA-B27 and the B7-CREG alleles in characterization and disease progression

OBJECTIVE: To analyze the profile of the HLA-B27 and B7 cross-reactive group (CREG) alleles and the role of these markers in disease characterization and progression in patients with undifferentiated spondyloarthropathies (uSpA). METHODS: A total of 80 patients with a diagnosis of uSpA (40 HLA-B27 positive and 40 HLA-B27 negative) were prospectively studied for 2 years. The control group consisted of 66 HLA-B27 positive and 112 HLA-B27 negative individuals without a history of seronegative SpA. HLA-B alleles were typed at low (B7-CREG alleles, i.e., B*7, B*54, B*55, B*56, B*40, B*42) or high resolution (B*27 alleles) using polymerase chain reaction-amplified DNA hybridized with sequence-specific oligonucleotide probes. RESULTS: HLA-B*2705 was the most frequent allele, observed in 92.5% of the patients and in 77% of the controls, followed by the HLA-B*2702, observed in 5% of the patients and in 12% of the controls. HLA-B*2704 was observed in only one patient (2.5%), and was absent in the control population. HLA-B*2703 (6%) and HLA-B*2707 (5%) alleles were observed only in controls. No associations between HLA-B*27 alleles or B7-CREG alleles and any specific manifestation of uSpA were observed. HLA-B27 positive patients more frequently presented juvenile onset SpA (p = 0.002) and progression to ankylosing spondylitis (AS) (p = 0.03) than did HLA-B27 negative patients. The B7-CREG alleles were observed in 5% of the HLA-B27 positive uSpA group, in 25% of the HLA-B27 negative uSpA group, in 7% of the HLA-B27 positive controls, and in 13% of the HLA-B27 negative controls; a significant association was observed between the presence of the B7-CREG and the HLA-B27 negative uSpA group (p = 0.012). CONCLUSION: The frequency of the HLA-B*2705 allele among the B27 positive uSpA patients of this series was closely similar to that reported for patients with ankylosing spondylitis (AS). The presence of HLA-B*27 alleles was associated with the progression to AS, and the presence of B7-CREG was associated with uSpA in the HLA-B27 negative group.     

Finnish HLA studies confirm the increased risk conferred by HLA-B27 homozygosity in ankylosing spondylitis

OBJECTIVE: To determine the influence of HLA-B27 homozygosity and HLA-DRB1 alleles in the susceptibility to, and severity of, ankylosing spondylitis in a Finnish population. METHODS: 673 individuals from 261 families with ankylosing spondylitis were genotyped for HLA-DRB1 alleles and HLA-B27 heterozygosity/homozygosity. The frequencies of HLA-B27 homozygotes in probands from these families were compared with the expected number of HLA-B27 homozygotes in controls under Hardy-Weinberg equilibrium (HWE). The effect of HLA-DRB1 alleles was assessed using a logistic regression procedure conditioned on HLA-B27 and case-control analysis. RESULTS: HLA-B27 was detected in 93% of cases of ankylosing spondylitis. An overrepresentation of HLA-B27 homozygotes was noted in ankylosing spondylitis (11%) compared with the expected number of HLA-B27 homozygotes under HWE (4%) (odds ratio (OR) = 3.3 (95% confidence interval, 1.6 to 6.8), p = 0.002). HLA-B27 homozygosity was marginally associated with reduced BASDAI (HLA-B27 homozygotes, 4.5 (1.6); HLA-B27 heterozygotes, 5.4 (1.8) (mean (SD)), p = 0.05). Acute anterior uveitis (AAU) was present in significantly more HLA-B27 positive cases (50%) than HLA-B27 negative cases (16%) (OR = 5.4 (1.7 to 17), p<0.004). HLA-B27 positive cases had a lower average age of symptom onset (26.7 (8.0) years) compared with HLA-B27 negative cases (35.7 (11.2) years) (p<0.0001). CONCLUSIONS: HLA-B27 homozygosity is associated with a moderately increased risk of ankylosing spondylitis compared with HLA-B27 heterozygosity. HLA-B27 positive cases had an earlier age of onset of ankylosing spondylitis than HLA-B27 negative cases and were more likely to develop AAU. HLA-DRB1 alleles may influence the age of symptom onset of ankylosing spondylitis.     

Clinical phenotype is related to HLA genotype in the peripheral arthropathies of inflammatory bowel disease

BACKGROUND & AIMS: The detection of phenotype-determining genes as opposed to disease susceptibility genes requires precise phenotypic characterization of patients. Peripheral arthropathies in inflammatory bowel disease (IBD) are well recognized and are classified with the HLA-B*27-related spondyloarthropathies by the European Spondyloarthropathy Study Group. However, previous HLA studies in IBD have only shown this association with axial disease rather than peripheral arthropathy. We recently reported a clinical classification that describes 2 types of peripheral arthropathy, distinguished by their natural history and articular distribution. We now report the results of immunogenetic studies in these patients and compare them with other spondyloarthropathies. METHODS: IBD patients with type 1 (n = 57) and type 2 (n = 45) peripheral arthropathy were identified by case note review and questionnaire. Patients and 603 controls from Oxfordshire were assigned HLA-A, -B, -C, -DR, and -DQ genotypes by sequence-specific primer polymerase chain reaction. Patient results were compared with controls (corrected for multiple comparisons), then with each other in light of existing hypotheses. The results were compared with those of a cohort of 30 patients with postenteric reactive arthritis (ReA) and 16 patients with IBD-associated ankylosing spondylitis (IBD-AS). RESULTS: Type 1 arthropathy was associated with HLA-DRB1*0103 (DR103; a rare subtype of DR1) in 33% (P < 0.0001; relative risk [RR], 12.1), B*35 in 30% (P = 0.01; RR, 2.2), and B*27 in 26% (P = 0. 001; RR, 4.0). In contrast, type 2 was associated with HLA-B*44 in 62% (P = 0.01; RR, 2.1). Similar significant associations to type 1 arthropathy were found in ReA, except that the HLA-B*27 association was significantly stronger and an association was found with DRB1*0101 (DR1) in 43% (P = 0.001; RR, 2.2). IBD-AS was associated only with HLA-B*27 and DRB1*0101. CONCLUSIONS: These data suggest that the clinical classification into type 1 and type 2 arthropathies describes immunogenetically distinct entities and establish that in polygenic disorders, genes may determine clinical phenotype without conferring overall disease susceptibility (in this case, HLA genes). Type 1 arthropathy is clinically and immunogenetically similar to the spondyloarthropathies, but different HLA associations may define phenotypically distinct groups. Type 2 arthropathy has different HLA associations and may have a different etiology. Further studies are now required to confirm these associations and to elucidate the different pathogenetic mechanisms.     

An antiserum to a disease-associated factor from the cells of an HLA-B27 positive patient with ankylosing spondylitis specifically recognizes an HLA-B27 associated determinant

Antiserum raised to a factor elaborated by a lymphoblastoid cell line derived from the peripheral blood cells of an HLA-B27 positive patient with ankylosing spondylitis specifically lyses the B27 positive, but not the B27 negative, cells of ankylosing spondylitis patients. The cells of B27 positive and B27 negative normal controls are not lysed. This serum has similar specificity to antisera against cross-reactive bacteria.     

A subgroup of ankylosing spondylitis associated with HLA-B7 in American blacks

In a study of 34 American black patients with primary ankylosing spondylitis, 18 were found to be HLA-B27-negative. Of these, 10 possessed HLA-B7 (55.6%) compared to 23.7% of 59 B27-negative black controls (P less than 0.025, relative risk = 4). On comparing these 10 B7-positive patients (group I) with 16 B27-positive black patients (group II), a difference in mean age at onset of disease was found: 33.6 years in group I and 22.2 years in group II (P less than 0.005). In addition, a family history of ankylosing spondylitis was absent in group I patients but present in 6 patients in group II (P = 0.034). These findings indicate an association between HLA-B7 and ankylosing spondylitis in American blacks and suggest that these patients who lack B27 but possess B7 represent a subgroup of patients with this disease.     

Sacroiliitis in psoriasis: relationship to peripheral arthritis and HLA-B27

One hundred and eighty-one patients attending a dermatology clinic were studied. Twenty-two (12%) were B27 positive. Twenty had peripheral psoriatic arthritis; 3 of these showed sacroiliitis (1 B27 positive, 2 B27 negative). Only one of the other 161 patients had sacroiliitis and he was B27 positive. Subsequently we examined 54 consecutive patients with psoriatic arthritis: 51 had peripheral arthritis (6 with sacroiliitis) and 3 exclusively axial involvement (2 sacroiliitis, one syndesmophytes with normal sacroiliac joints). All patients were pooled together and divided in 4 groups: B27 positive and negative, with or without peripheral arthritis. HLA-B27 and/or peripheral arthritis were associated with an increase in axial involvement. Patients lacking both B27 and peripheral arthritis did not have sacroiliitis and only in one case showed evidence of spinal disease (0.7%). Half of the patients with peripheral arthritis and spinal involvement were B27 positive. All 3 B27 positive patients without peripheral arthritis and with spinal disease were men and they all had bilateral sacroiliitis, indistinguishable from idiopathic ankylosing spondylitis (AS). HLA-B27 and peripheral arthritis appeared to act as separate factors that increased the risk of spinal arthritis in patients with psoriasis. The effect of B27 on psoriasis appeared to be detected in 2 different ways: as a coincidental factor increasing the risk of idiopathic AS (as for the general population) or as one of the multiple HLA associations that increase the risk of psoriatic arthritis; in this latter case the spinal involvement could occur as another manifestation of the clinical course of the disease.     

Spinal abnormalities similar to ankylosing spondylitis in a 58-year-old woman with ochronosis

Summary Ochronotic arthropathy (spondylosis or peripheral arthropathy) is a late complication of alkaptonuria. There is a tendency for HLA-B27 positive patients with alkaptonuria to develop ochronotic spondylosis. A 58-year-old white woman, presented with ochronotic spondylosis. She was HLA-B27 positive. Her family history was positive for alkaptonuria. Ochronotic patients with HLA-B27 positivity develop spinal changes similar to ankylosing spondilitis (AS).     

LMP2 polymorphism is associated with extraspinal disease in HLA-B27 negative Caucasian and Mexican Mestizo patients with ankylosing spondylitis

OBJECTIVE: To determine the effects of HLA Class II genes, particularly LMP2 and previously implicated Class I genes, on susceptibility and disease expression in HLA-B27 negative ankylosing spondylitis (AS). METHODS: Patients included 41 HLA-B27 negative Caucasians from a total AS population of 546 and 17 HLA-B27 negative Mexican Mestizo. Controls included 4352 random HLA-B27 negative Caucasians. LMP2 genotype assignments were made on all patients and 282 random Caucasian controls by polymerase chain reaction-restriction fragment length polymorphism with the Cfo I restriction enzyme while HLA typing was performed on patients and controls using microcytotoxicity assays for Class I, and sequence specific probe-PCR for HLA-B60, B39, B38, and DR. RESULTS: The LMP2BB genotype was significantly decreased in Caucasian AS patients without extraspinal (ES) disease (25%) compared to AS patients with ES (64.7%) (p = 0.01) and random Caucasian controls (53.9%) (p = 0.007), even when those with colitis and psoriasis were excluded from analysis (ES+ 55.6% versus ES- 22.2%). This finding remained significant after stratification by HLA-DR. Similar trends were noted in the Mexican population. A potential role for HLA-DR8 and DR2 in susceptibility to disease was observed in Caucasian patients, although this observation requires confirmation. We could not confirm reported associations with HLA-B60 or B39. Peripheral arthritis was significantly more commonly observed in those who had had acute anterior uveitis (AAU) (75%) than in those who had not developed AAU (27.3%) (p = 0.04). CONCLUSION: HLA Class II encoded genes may have effects on disease susceptibility and/or phenotype in HLA-B27 negative individuals similar to those noted in HLA-B27 positive AS. Eccentric and axial phenotypes of disease may be immunogenetically determined.     

TNF-238A promoter polymorphism contributes to susceptibility to ankylosing spondylitis in HLA-B27 negative patients.

OBJECTIVE: To investigate the relative contribution of MHC loci in their susceptibility to primary ankylosing spondylitis (AS) in HLA-B27 negative patients and to compare the clinical features and genetic factors with those of HLA-B27 positive AS. METHODS: DNA from patients with B27 negative primary AS (n = 28), B27 positive primary AS (n = 77), and matched healthy controls (B27-, n = 100; B27+, n = 70) were analyzed to investigate whether HLA genes determine the disease susceptibility, or whether other closely linked loci might play a role in disease development. HLA typing was carried out by serology and PCR/SSP (HLA-B, -DR), MICA-TM polymorphism in the transmembrane region by radioactive PCR, and tumor necrosis factor-alpha (TNF-alpha) promoter polymorphism at positions -238 and -308 by PCR-RFLP. RESULTS: Subtle clinical differences were found for primary AS, the B27 negative patients being less frequently complicated by acute anterior uveitis and more associated with peripheral arthritis than B27 positive. Differences were found in the distribution of TNF-alpha -238 genotypes among patients with primary AS (B27- vs B27+). The TNF-alpha -238(A) polymorphism was present in 50% of the B27 negative patients carrying the -238 G/A and A/A genotypes and was significantly increased compared with B27 positive AS (odds ratio 4.3) and with the B27 negative control group (OR 5.9). The TNF-alpha genotypes were equally prevalent in B27 positive AS and healthy matched B27 positive controls. No significant HLA and MICA typing differences were found between the populations under study. CONCLUSION: Our results indicate that the polymorphism variation in the TNF-alpha promoter -238.2(A) influences disease susceptibility in B27 negative primary AS but had no effect in our B27 positive AS population.     

HLA class II antigens (DR, DQ loci) and peripheral arthritis in ankylosing spondylitis.

Fifty one patients with ankylosing spondylitis (AS) were typed for HLA-A, B, C, DR, and DQ antigens. The antigen frequencies were compared with those of a normal population and with a B27 positive control group. All but one of the patients with AS were HLA-B27 positive. A positive linkage disequilibrium between Cw1, Cw2, DR1, and the B27 antigen was observed. Patients with AS showed a significant increase in DQw2 antigen compared with the B27 positive control group. No differences in antigenic frequencies were observed in patients having peripheral arthritis and patients with only axial involvement. Seven out of nine patients (78%) with an erosive peripheral arthritis were DR7 positive, suggesting that DR7 or genes closely linked could be related with a more aggressive peripheral joint involvement in patients with AS.     

Two-dimensional gel analysis demonstrates no structural alteration of HLA-B27 polypeptides between patients with ankylosing spondylitis and healthy individuals.

After precipitation of the HLA-B27 antigen from the surface of peripheral blood lymphocytes (PBL) by means of an anti-HLA-B27 allospecific monoclonal antibody 2-dimensional gel electrophoresis was used to compare the structure of the B27 antigens derived from 5 patients with ankylosing spondylitis with that of healthy HLA-B27 positive counterparts. No significant difference in polypeptide structure was noted, which suggests that the pathogenesis of ankylosing spondylitis does not involve a structural alteration in cell surface HLA-B27 molecules.     

Sacroiliitis detected by bone scintiscanning: a clinical, radiological, and scintigraphic follow-up study.

Twenty-four patients had abnormal sacroiliac joints detected by quantitative sacroiliac scintigraphy but no radiological evidence of sacroiliitis on original investigation. We studied them again after intervals of 12 to 36 months. Four patients developed radiological change. Two young, HLA B27-positive men had undoubted ankylosing spondylitis, and a young woman had possible ankylosing spondylitis. A middle-aged man had changes that could be attributed to post-traumatic osteoarthrosis. Of the remaining 20 cases 15 had symptoms and signs suggestive of inflammatory disease of the axial skeleton (and peripheral arthropathy in 5 cases). The sexes were affected equally (8 females, 7 males), and only 2 of the 15 were B27-positive. The response to anti-inflammatory medication was generally good to excellent, and scintiscans tended to improve. Of the remaining 5 patients, 3 had mechanical or traumatic problems, and in 2 there was no explanation for the abnormal sacroiliac scintiscan. We conclude that quantitative sacroiliac scintigraphy may detect ankylosing spondylitis prior to the develpment of radiological change and that it can identify an organic basis for backache in patients with a spondylitis-like syndrome. The clinical circumstances must be taken into account, as scintigraphic abnormalities are not diagnostic of any specific disease entity.     

Apical pulmonary fibrosis in psoriasis

Apical pulmonary fibrosis has been established as a non-articular complication of ankylosing spondylitis. Although psoriasis is frequently associated with arthropathy and spondylitis, there is only one previous report of apical fibrosis occurring in a patient with psoriasis. We report two patients with psoriasis complicated by apical pulmonary disease in whom extensive investigations were negative.     

Low T cell production of TNFalpha and IFNgamma in ankylosing spondylitis: its relation to HLA-B27 and influence of the TNF-308 gene polymorphism

OBJECTIVE: To test the hypothesis that ankylosing spondylitis (AS) is a T helper cell type 2 polarised disease by quantifying the T cell cytokines interferon gamma (IFNgamma), interleukin 4 (IL4), tumour necrosis factor alpha (TNFalpha), and IL10 at the single cell level in patients with AS in comparison with healthy HLA-B27 negative and HLA-B27 positive controls. METHODS: Peripheral blood mononuclear cells from 65 subjects (25 HLA-B27 positive patients with active AS, 18 healthy HLA-B27 positive controls, and 22 healthy HLA-B27 negative controls) were stimulated with phorbol myristate acetate/ionomycin for six hours, surface stained for CD3 and CD8, intracellularly stained for the cytokines IFNgamma, TNFalpha, IL4, and IL10, and analysed by flow cytometry. TNFalpha production was related to the genotype of the TNFalpha promoter at the -308 and -238 polymorphisms. RESULTS: In peripheral blood the percentage of TNFalpha+ T cells was significantly lower in HLA-B27 positive patients with AS (median 5.1% for CD4+ T cells) than in healthy HLA-B27 negative controls (median 9.5%; p=0.008). Surprisingly, the percentage of TNFalpha+ T cells was also significantly lower in healthy HLA-B27 positive controls (median 7.48%) than in healthy HLA-B27 negative controls (p=0.034). Furthermore, the percentage of IFNgamma+ T cells was lower in patients with AS and in healthy HLA-B27 positive controls than in healthy HLA-B27 negative controls (p=0.005 and p=0.003, respectively). The percentage of IL10+/CD8+ T cells was higher in patients with AS than in both control groups. In HLA-B27 positive subjects, TNF1/2 heterozygosity at -308 (n=6) was associated with a higher percentage of TNFalpha+ T cells than TNF1/1 homozygosity (n=25; median 9.97% v 5.11% for CD4+ T cells; p=0.017). In contrast, in HLA-B27 negative controls (n=18) there was no such genotype/phenotype correlation (median 9.4% v 10.6%). CONCLUSIONS: The lower T cell production of TNFalpha and IFNgamma shown at the single cell level in HLA-B27 positive patients with AS and healthy HLA-B27 positive controls may contribute to the increased susceptibility of HLA-B27 positive subjects to develop AS. Preliminary genotype-phenotype correlations suggest that in HLA-B27 positive subjects TNF2 at -308 or a linked gene results in higher TNFalpha production and, therefore, might be a marker for a protective haplotype.     

Measurement of HLA class I expression in ankylosing spondylitis.

The importance of HLA-B27 in the pathogenesis of ankylosing spondylitis is uncertain: current evidence favours a role for the B27 molecule itself. The possibility that quantitative differences in HLA-B27 expression may exist between patients with ankylosing spondylitis, family members, and control subjects positive for B27 was examined using appropriate monoclonal antibodies, flow cytometry, and a 'model lymphocyte' coated with a known number of mouse immunoglobulin binding sites. No differences were found between the groups. HLA-A2, examined for comparison, was expressed in greater amounts than HLA-B27, but each contributed only 10-20% of the total class I antigens. Homozygotes expressed twice the amount of antigen expressed by heterozygotes. Synovial lymphocytes expressed more class I antigens than peripheral lymphocytes.