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Results for “HLA-B51 Antigen”

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At least 19 recordsLinked to original sources
PubMed1992

Idiopathic childhood stroke is associated with human leukocyte antigen (HLA)-B51.

We report four children with idiopathic stroke syndromes who were assayed for human leukocyte antigen (HLA) class I markers and found to have HLA-B51 in common. This finding suggests that there may be a genetic predisposition for "idiopathic" childhood stroke, and host factors, possibly in concert with environmental factors or viruses, may play a major role in the mechanism of unexplained occlusion of the cerebral vasculature in children.

Cerebrovascular Disorders↗
PubMed1992

Close association of HLA-B51 in persons with recurrent aphthous stomatitis.

The HLA typing profile of 26 Israeli subjects with recurrent aphthous stomatitis (RAS) was examined and compared with that of 100 healthy control subjects. HLA-B51 was found in six subjects (23%) with RAS and in nine control subjects (9%) (p < 0.05). HLA-Cw7 was found in six subjects with RAS (23%) and in five control subjects (5%) (p < 0.01). Eleven subjects had first-degree relatives who had RAS. Because a high frequency of HLA-B51 has been found in Behcet's syndrome and aphthous stomatitis is part of this syndrome, it is suggested that in some subjects with RAS the entire syndrome may actually develop in the future.

Adolescent↗
PubMed1992

Association of HLA-B51 and lack of association of class II alleles with Behçet's disease.

Eighty-one Behcet's disease patients have been studied for HLA association by HLA-DRB1, -DQA1, -DQB1 and -DPB1 genotyping with the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and for NcoI RFLP in the tumor-necrosis factor (TNF beta) gene by Southern hybridization in addition to serological typing. In serological typing, the frequency of HLA-B51 was significantly increased in the patients. In PCR genotyping, there was a significant increase in the HLA-DRB1*0802, DQA1*0301 and DQB1*0303 alleles, whereas the frequencies of DRB1*1502, DQA1*0103, DQA1*0101, DQB1*0601 and DQB1*0501 showed a significant decrease in the patients. No significant difference was observed in any HLA-DPB1 alleles. Among them, B51 was found to be a genetic marker most strongly associated with Behcet's disease (p less than 0.00005, chi 2 = 46.47, pc[corrected p] less than 0.005). The positive and negative associations of class II alleles with the disease can be explained by linkage disequilibrium with B51, and do not reach statistical significance by the corrected p-value test. In NcoI RFLP typing in the TNF beta gene, 250 kb centromeric of the HLA-B gene, the frequency of a 5.5 kb fragment was considerably decreased in the patients when compared to the controls, although the decrease was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1992

Histocompatibility antigens associated with Behçet's disease in northern Han Chinese.

Among Han nationality Chinese and living in the northern area of the Yellow River, 120 patients suffering from Behçet's disease and 100 unrelated healthy individuals were typed for histocompatibility antigens (HLA)-A, -B, -C, and -DR and -DQ antigens. HLA-DR and DQ typing was performed on B-lymphocyte separated with Lympho-B-Kwik. The HLA-antisera were provided by 11th IHWC. Bf alleles and C4 allotypes were determined by immunofixation agarose-gel electrophoresis. HLA-B51 was found in 67/120 (55.83%) patients and in 12/100 (12%) controls, the Chi-square and relative risk values were 45.54 and 9.27, respectively (p < 0.0005). C4AQ0 frequency was significantly increased in the patient group. In the complete form group HLA-B51 was observed more frequently (62.79%). No significant differences of other HLA antigens, frequencies, Bf or B4 alleles were found between the groups.

Adult↗
PubMed1992

Human leukocyte antigen serologic and DNA typing of Behçet's disease and its primary association with B51.

Ninety Japanese patients with Behçet's disease (BD) were typed for human leukocyte antigen (HLA)-DRB1, -DQA1-, -DQB1, and -DPB1 alleles by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and for HLA-A, -B, -C, -DR, and -DQ antigens by conventional serologic typing. Serologic HLA typing showed a remarkably significant increase of HLA-B51 and a significant decrease of HLA-DQw1 in the patients with BD, especially those with ocular lesions including complete type, as compared with the control group (for B51, chi-squared = 46.75, P corrected < 0.001, relative risk [RR] = 7.9; for DQw1, chi-squared = 12.10, P corrected < 0.01, RR = 0.4). By PCR-RFLP genotyping, no significant difference was revealed in any class II alleles between the patient and the control groups in the corrected P value test, but P value analysis showed the significantly high frequency of DRB1*0802 and the significantly low frequencies of DQA1*0103, DQB1*0601, and DQB1*0501. No significant difference was observed in any DPB1 alleles by either P value analysis. These results indicated that the primary and primordial gene(s) responsible for the susceptibility to BD, especially related to ocular lesions, were not located in the HLA class II gene region but were in or very close to the HLA-B locus in the class I region. They also suggested the possibility that BD was a symptom complex associated with some independent diseases.

Alleles↗
PubMed1992

Effect of the substitutions in the alpha helix and the beta sheet of HLA class I molecule on allorecognition of T cells specific for HLA-B51 and HLA-Bw53.

HLA-B51 and HLA-Bw53 differ by eight amino acids on the alpha 2 domain. Of these eight amino acid substitutions, two are in the alpha helix and six are in the beta sheet. The effect of these substitutions on allorecognition of HLA-B51-specific cytotoxic T lymphocyte (CTL) clones and HLA-Bw53-specific CTL clones was investigated using chimeric antigen (Ag) between HLA-B51 and HLA-Bw53. Of 12 HLA-B51-specific CTL clones, recognition of one clone was abolished by the substitutions on the beta sheet alone, that of two clones by the substitutions on the alpha helix alone, and that of nine clones not only by the substitutions on the alpha helix but also by those on the beta sheets. On the other hand, of 17 HLA-Bw53-specific CTL clones, recognition of 10 clones was affected by the substitutions on the alpha helix alone and that of 7 clones not only by the substitutions on the alpha helix but also by those on the beta sheet. The present study demonstrated that the substitutions (residues 152 and 171) on the alpha helix critically affect recognition of HLA-B51-specific CTL clones and HLA-Bw53-specific CTL clones and that the substitutions on the beta sheet affect also recognition of the majority of HLA-B51-specific CTL clones and 40% of HLA-Bw53-specific CTL clones. These results indicate that the substitutions at the floor of the peptide binding groove affect recognition of allogeneic CTL.

Amino Acid Sequence↗
PubMed1991

[Association of HLA antigens with thyrotoxic periodic paralysis].

Periodic paralysis is a rare and peculiar complication of thyrotoxicosis, especially in Chinese and Japanese patients. The susceptibility to autoimmune thyroid disease has recently been reported to be strongly linked with certain immunogenetic factors. The objective of this study was to seek a genetic marker by HLA typing in Chinese patients with thyrotoxic periodic paralysis (TPP). The distribution of HLA-A, B, C, DR and DQ antigens in 20 thyrotoxic patients with periodic paralysis and 51 thyrotoxic patients without periodic paralysis was compared with that in 100 controls. The results showed that among the patients with TPP, these was a highly significantly increase of HLA-B51 frequency and B51 appeared to be linked with Cw3 in a state of dysequilibrium.

Adult↗
PubMed1992

Increased peripheral blood gamma delta+ T cells and natural killer cells in Behçet's disease.

Peripheral blood cytotoxic lymphocytes, including gamma delta+ T cells, natural killer (NK) cells, and CD56+ T lymphocytes were investigated by using 2-color flow cytometry in patients with Behçet's disease. The percentage of circulating gamma delta+ T cells among total lymphocytes or among total T cells was significantly increased in patients with Behçet's disease, compared to healthy controls. An increase in circulating gamma delta+ T cells was related to mucocutaneous lesions, but not the HLA-B51. Among gamma delta+ T cells, the number of CD8+ or CD56+ subset was significantly increased in patients with Behçet's disease. Moreover, significant increases of peripheral blood NK cells (CD16+CD56+CD3-, CD2+CD3-, CD8dim+CD3-) and CD56+ T lymphocytes were also observed. Our data suggest that increased circulating gamma delta+ T cells and NK cells may play an important role in the pathogenesis of Behçet's disease.

Adult↗
PubMed1992

Streptococcal-related antigens stimulate production of IL6 and interferon-gamma by T cells from patients with Behcet's disease.

Greater attention has been recently paid to the role of certain strains of streptococcus as an etiologic agent of Behçet's disease, in which T cell abnormalities are considered to be involved. We therefore examined whether T cells from patients with Behçet's disease might to be stimulated by Streptococcus sanguis-related antigen (RRE KTH-1 antigens). T cells from 17 patients with Behcet's disease, but not those from 13 healthy individuals or from 13 patients with other rheumatic diseases, were stimulated to produce greater amounts of interleukin 6 (IL6) by addition of RRE KTH-1 antigens [stimulation index: 3.96 +/- 0.56 and 1.35 +/- 0.28 or 1.83 +/- 0.43 (mean +/- SEM), respectively]. The IL6 production by T cells required the presence of either fresh or paraformaldehyde-fixed monocytes. The enhancement of T cell IL6 production was not related to the presence of HLA-B51, which has been shown to be frequently associated with Behçet's disease. These results indicate that T cells from patients with Behçet's disease are stimulated by streptococcal antigens to produce IL6 through T cell-monocyte interactions in which binding of the antigens to monocytes, but not necessarily processing of the antigens by monocytes, is involved. Moreover, RRE KTH-1 antigens as well as Escherichia coli-derived antigens also enhanced the production of interferon-gamma by T cells from patients with Behçet's disease. The data thus suggest that T cell hypersensitivity to several bacterial antigens may play a central role in the pathogenesis of Behçet's disease.

Adult↗
PubMed1992

Two subtypes of HLA-B51 differing by substitution at position 171 of the alpha 2 helix.

Newly defined antigens of the B5, B35 cross-reacting group have been found in Japanese and North American Indians. Nucleotide sequencing of the alleles encoding the Japanese B5.35 antigen and the variant B5 antigen from the Piman Indians show them to be identical. This new allele, B*5102, differs from B*5101 by a single nucleotide substitution that changes residue 171 from histidine to tyrosine. Residue 171, which is part of the alpha 2 helix, is believed to contribute directly to peptide interaction in the A pocket of the binding groove and is either histidine or tyrosine in all HLA-A, B, C heavy chains. Tyrosine 171 is shared by B*5102, B*3501, B*3502, and B*5301 and must be responsible for the serological cross-reactivities of these molecules not shared with B*5101. Stimulation of lymphocytes from a B*5101 positive donor with B*5102 positive cells failed to generate cytotoxic T cells with specificity for the difference between these molecules. However, one out of five clones of cytotoxic T cells raised against B*5101 failed to lyse targets expressing B*5102. Substitution of histidine for tyrosine at residue 171 affected recognition of HLA-B35-restricted human minor histocompatibility antigen-specific T cell clones.

Amino Acid Sequence↗
PubMed1992

RFLP analysis in the TNF-beta gene and the susceptibility to alloreactive NK cells in Behçet's disease.

Behçet's disease is known to be associated with HLA-B51. To address the possibility that a non-human leukocyte antigen (HLA) gene closely linked to the HLA-B gene, such as tumor necrosis factor (TNF)-alpha, TNF-beta, or ECl (the locus that determines the susceptibility to alloreactive natural killer [NK] cells), is involved in the susceptibility to Behçet's disease, NcoI and EcoRI restriction fragment length polymorphisms in the TNF-beta gene and the susceptibility to lysis by alloreactive NK cells were investigated in Behçet's patients. In our NcoI restriction fragment length polymorphism (RFLP) analysis in the TNF-beta gene, the frequency of the NcoI 5.5 kb homozygote was decreased considerably in the patients, especially those with the ocular lesions, in relation to the healthy controls. However, no significant difference was observed between these groups in the EcoRI RFLP band distribution in this gene or the in susceptibility to lysis by alloreactive NK cells. These results indicated that a non-HLA gene located around the TNF gene region centromic of the HLA-B gene was a candidate to control the genetic susceptibility to Behçet's disease.

Base Sequence↗
PubMed1992

Conservation of genes encoding HLA-B5 and B35 cross-reactive group antigens in various races.

HLA-B5 and B35 CREG antigens include HLA-B35, B51, B52, B53, and B78. Recent studies suggest that the genes encoding the HLA-B5, B35 CREG, and HLA-B58 antigens share a common ancestor. We sequenced the exons of the genes encoding HLA-B51, B53, and B58 from American black individuals and the gene HLA-B52 encoding from an Arabic individual, and compared them with previously reported sequences of HLA-B51 (B*5101) and HLA-B52 (B*5201) from Japanese, HLA-B53 (B*5301) from an Algerian, and HLA-B58 (B*5801) from a Sardinian. The sequences of the genes from the American black and Arabic individuals were identical to those from the other races. These findings support the hypothesis that these antigens have evolved prior to divergence of the major ethnic groups.

Base Sequence↗
PubMed1990

Differential regulation of HLA class I genes by interferon.

Allele-specific differences in the regulation of HLA class I genes by type I interferon (IFN) were observed after transfection of eight HLA-B, -A, or -C genes into mouse L cells. HLA-B7 and -Bw64 gene expression was significantly more inducible by type I IFN than the genes coding for HLA-B27, HLA-B51, HLA-B38, HLA-B39, HLA-Cw3, and HLA-A2 antigens. Modification of the 5' end of HLA-B7 and HLA-B27 genes revealed the presence of enhancer sequences responding to IFN treatment in the 5' untranslated region of HLA-B7, but not of HLA-B27 and suggested further, independently acting enhancer elements downstream of the transcription initiation site. Comparison of 5' enhancer region sequences in correlation with type I IFN inducibility of the different HLA class I alleles indicated that the exchange of only two nucleotides in the interferon response sequence (IRS) or enhancer A region of HLA-B7 or -Bw64 could account for nonregulated promoters in all other HLA-A, -B, or -C alleles analyzed. Thus, type I IFN stimulation of HLA class I genes in mouse L cells appears to predominantly operate in most alleles by a mechanism targeted to enhancer sequences downstream of the gene's transcription initiation site.

Alleles↗
PubMed1991

T cell can recognize the allospecificities formed by the substitution of amino acids associated with HLA-Bw4/Bw6 public epitopes.

Our previous studies clearly showed that HLA-B35 and HLA-Bw53 differed only by the amino acids associated with HLA-Bw4/Bw6 epitopes, in that the former possessed Bw6 and the latter Bw4 epitope. It remains to be known whether T cell can discriminate HLA-B35 from HLA-Bw53, although the difference between these HLA antigens is discriminated by monospecific human alloantisera. To investigate allorecognition of these HLA antigens by T cells, anti-HLA-Bw53 cytotoxic T lymphocytes (CTLs) were generated. Anti-HLA-Bw53 cytotoxic T lymphocytes (CTLs) were generated. Anti-HLA-Bw53 bulk CTLs from an individual with HLA-B35 clearly discriminated HLA-Bw53 from HLA-B35. On the other hand, anti-HLA-Bw53 bulk CTLs from an individual without HLA-B35 revealed weak cross-reactivity with HLA-B35 and HLA-B51. The additional studies using HLA-Bw53 or HLA-B35-specific CTL clones showed that some but not all of the CTL clones definitively distinguish the difference between HLA-Bw53 and HLA-B35. Thus, the allospecificities formed by HLA-Bw4/Bw6 epitopes were discriminated by allogeneic T cells. The present study demonstrated that HLA-Bw4/Bw6 public epitopes play an important role in allorecognition of T cells.

Amino Acid Sequence↗
PubMed1992

Familial Behçet's disease.

OBJECTIVES: To highlight the frequency, clinical features and histocompatibility antigen types of the familial form of Behçet's disease. METHODS: Twenty-seven cases with familial Behçet's disease in 12 families were evaluated according to clinical features, sites of involvement, HLA-A and HLA-B typing. A review of the literature is presented. RESULTS: The frequency of familial form of Behçet's disease was found to be 8.7% among 137 patients studied. Vascular involvement was 7.4% (2/27) in the familial group while it was 28.8% (36/125) in patients without the familial form of the disease (p < 0.01). HLA-B51(5) and HLA-A2 were positive in 68% and 75% in 16 familial cases studied, respectively. CONCLUSIONS: Familial Behçet's disease, which constitutes a small group of patients with Behçet's disease, may represent a clinically heterogeneous subtype of this entity. Although lower frequency of vascular complications was observed in this study, it is not possible to indicate the precise frequency of vascular and ocular complications of the familial form of Behçet's disease. The frequencies of HLA-A2 and HLA-B51(5) positivity are higher than the previously reported non-Behçet's controls from Turkey.

Adolescent↗