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PubMed1986

Analysis by sequential immunoprecipitations of the specificities of the monoclonal antibodies TU22,34,35,36,37,39,43,58 and YD1/63.HLK directed against human HLA class II antigens.

The monoclonal antibodies (MOABs) TU22, TU34, TU35, TU36, TU37, TU39, TU43, TU58 and YD1/63.HLK were used to identify subpopulations of class II antigens encoded by the human major histocompatibility complex. Since all MOABs reacted with B lymphocytes of HLA-DR1-8 homozygous as well as all heterozygous cells tested, they recognize monomorphic determinants, with the possible exception of TU58 and YD1/63.HLK which do not fix complement. As shown by radioactive binding assays and immunoprecipitations of labeled chains, 3 MOABs reacted strongly and 3 others weakly with isolated beta-chains, and the former also bound alpha-chains, albeit very weakly. Immunoprecipitations with the MOABs from 125I-labeled KR3598 cells (Dw5, DR5, MT2, MB3 homozygous, SB2, SB4) demonstrated that at least 4 different subpopulations of class II antigens were present in the lysate. Possibilities to reconcile these biochemical data with the reactivity of the MOABs with HLA mutant cell lines and with functional as well as tissue distribution studies are discussed.

Animals↗
PubMed2004

Role of HLA class II alleles in susceptibility to and protection from localized cutaneous leishmaniasis.

Localized cutaneous leishmaniasis (LCL) is the prevalent form of leishmaniasis in Mexico. It is limited to the skin; reversible upon treatment and the host cellular immune response is intact. Several genes that influence the expression of LCL have been described in the mouse. In humans, we, as well as others, have demonstrated that HLA-DQ3 antigens seem to play some role in host susceptibility. We therefore analyzed at the DNA level, the class II loci of the same patients that were previously studied by serology. The purpose of this study was to assess the contribution of HLA DR, DQ, and DP genes in the protection and/or the susceptibility to LCL. Sixty-five patients with LCL from Comalcalco, state of Tabasco, were recruited and 100 healthy controls were included for comparison. All were Mexican Mestizos. DRB1, DQA1, DQB1, DPA1, and DPB1 alleles were typed using two different methods: PCR-SSO and PCR-SSP. Results indicate that class II genes are relevant for the expression of LCL and several loci contribute independently and sinergically. DRB1*0407 participates in susceptibility with an etiological fraction (EF) of 20% and an odds ratio (OR) of 2.92. Two additional susceptibility genes were found. These are located to the DP locus: DPA1*0401 (OR = 10.07; EF=7%) and DPB1*0101 (OR = 5.99 EF = 13%). Resistance was found associated to DPB1*0401, thus *0401 "motif" could be an ideal candidate for the development of a vaccine. DR2 (DRB1*1500+DRB1*1600) has also a significant p for protection, suggesting that the sequence common to this group of antigens may anchor parasite peptides which trigger a protective response.

Alleles↗
PubMed1997

HLA class II haplotype and sequence analysis support a role for DQ in narcolepsy.

A systematic haplotype and sequencing analysis of the HLA-DR and -DQ region in patients with narcolepsy was performed. Five new (CA)n microsatellite markers were generated and positioned on the physical map across the HLA-DQB1-DQA1-DRB1 interval. Haplotypes for these new markers and the three HLA loci were established using somatic cell hybrids generated from patients. A four-marker haplotype surrounding the DQB1(*)0602 gene was found in all narcolepsy patients, and was identical to haplotypes observed on random chromosomes harboring the DQB1(*)0602 allele. Eighty-six kilobases of contiguous genomic sequence across the region did not reveal new genes, and analysis of this sequence for single nucleotide polymorphisms did not reveal sequence variation among DQB1(*)0602 chromosomes. These results are consistent with other studies, suggesting that the HLA-DQ genes themselves are among the predisposing factors in narcolepsy.

Causality↗
PubMed1983

Human allospecific T cell proliferative clones: different T cell clones expressing an apparently identical HLA class II specificity are heterogeneous in regard to their proliferative inhibition by a panel of monoclonal antibodies against human Ia-like antigens.

Four independent PLT clones displaying an apparently identical class II specificity (i.e., Dw/DR3) were found to give a heterogeneous pattern of inhibition in relation to 15 anti-class II mAb and an anti-beta 2m mAb used as a control. Some clones were inhibited by all anti-class II mAbs, irrespective of the cluster of molecular subsets with which they reacted. Such clones were also inhibited by the control anti-beta 2m mAb. Other clones were inhibited by only a few of the mAb tested. Within this group of T clones following the addition of a limiting amount of conditioned medium the inhibitory data of all independent clones with an identical specificity were inhibited by the same mAb; under these conditions, it was possible to relate the mAb inhibition patterns with the specificity of the T cell clones and these T cell specificities with the epitopic cluster/molecular subsets defined by these mAbs. A new level of T cell subset heterogeneity within T cell clones with apparent identical proliferative specificities is demonstrated, in relation to the T cell clone "susceptibility" or "resistance" to the effects of anti-class II mAbs directed towards their own Ia-like antigens.

Antibodies, Monoclonal↗
PubMed2006

Intranasal exposure to bacterial superantigens induces airway inflammation in HLA class II transgenic mice.

Staphylococcus aureus is widely prevalent in the nasopharynges of healthy individuals (carriers) but can also cause serious infections. S. aureus can elaborate a variety of superantigen exotoxins in "carrier" or "pathogenic" states. Streptococcus pyogenes can also colonize the nasopharynx and elaborate superantigens. Unlike the acute effects of superantigen exotoxins absorbed through the gut or vaginal mucosa, little is known regarding the pathogenesis of superantigens entering through the intranasal route. In the current study, we evaluated the local and systemic effects of staphylococcal enterotoxin B (SEB) and streptococcal pyrogenic exotoxin A (SPEA) delivered through the intranasal route. Superantigens were administered intranasally on multiple occasions, and experimental animals were sacrificed on day 8 for experimental analyses. SEB-induced airway inflammation was more pronounced for HLA-DR3 transgenic mice than for BALB/c mice, consistent with bacterial superantigens binding more efficiently to human than murine major histocompatibility complex class II. The nature of the airway inflammation in HLA-DR3 mice was determined by the concentration of SEB applied intranasally. Low concentrations (20 ng) induced eosinophilic airway inflammation as well as eosinophil degranulation, whereas intranasal exposure to higher concentrations (2,000 ng) resulted in neutrophilic airway inflammation, permanent airway destruction, toxic shock, and mortality. SEB-induced eosinophilic inflammatory response was enhanced in signal transducer and activator of transcription (STAT)-4-deficient HLA-DQ8 transgenic mice with defective interleukin-12 signaling. Intranasal administration of SPEA induced airway inflammation and systemic immune activation in HLA-DQ8 transgenic mice. In conclusion, repeated chronic intranasal exposure to bacterial superantigens causes airway inflammation and systemic immune activation.

Administration, Intranasal↗
PubMed2000

Antineutrophil cytoplasmic antibodies and HLA class II alleles in minocycline-induced lupus-like syndrome.

We report 14 patients with minocycline-induced lupus-like syndrome (four men, 10 women; mean age 27.8 years) who developed a lupus-like illness after chronic use of minocycline for acne (1-10 years, median 3.8). Clinical features resolved completely on drug withdrawal (mean follow-up 11 months) and reappeared in two patients who were rechallenged. Sera from all 14 patients contained antineutrophil cytoplasmic antibodies (ANCA) giving a perinuclear pattern on indirect immunofluorescence on ethanol-fixed human neutrophils (p-ANCA), whereas 14 control asymptomatic individuals taking minocycline for acne were ANCA-negative. Eleven of the 14 patients had elevated antimyeloperoxidase antibodies and 10 had antielastase antibodies on enzyme-linked immunosorbent assay, which diminished on extended follow-up, as did other serological abnormalities. Major histocompatibility complex class II typing demonstrated that all of the 13 patients tested were either HLA-DR4 (nine of 13) or HLA-DR2 (four of 13) positive, and all had an HLA-DQB1 allele encoding for tyrosine at position 30 of the first domain. Our findings suggest a model whereby the presence of p-ANCA may be a marker for the development of lupus-like symptoms in genetically susceptible individuals taking minocycline for acne.

Adolescent↗
PubMed1994

Lateral organization of the ICAM-1 molecule at the surface of human lymphoblasts: a possible model for its co-distribution with the IL-2 receptor, class I and class II HLA molecules.

Lateral distribution of the ICAM-1 molecule and its topological relationship (mutual proximity) to the heavy and light chains of class I HLA molecules, HLA-DR and interleukin-2 receptor alpha-chain (IL-2R alpha) were studied in the plasma membrane of HUT-102B2 T and JY B lymphoblastoid cell lines by the technique of flow cytometric energy transfer (FCET). Effects of adherency and treatments with recombinant interferon-gamma or tumor necrosis factor-alpha on the relative expression level of ICAM-1 to the above cell surface proteins were also investigated. While the cytokines did not significantly affect the ICAM-1 level of either cell line, an increased ICAM-1 expression was found on adherent JY cells. The ICAM-1 expression varied significantly with the cell cycle and culture conditions, as well. The statistical analysis of the differences observed in the energy transfer efficiency histograms resulted in a possible model of lateral co-distribution of these proteins in the plasma membrane. These two-dimensional patterns proved to be different for T and B lymphoma lines. ICAM-1 molecules showed a high degree of self-association on HUT-102B2 (T) cells, while they were mainly expressed as monomers on the surface of JY (B) cells. Both cells showed a significant (ca. 30%) difference between densities of the heavy and light chains of class I HLA antigen, suggesting a substantial amount of beta 2-microglobulin free heavy chains on these cell lines. The class I HLA molecules also showed partial self-association, but on both cell lines. The beta 2-microglobulin and the heavy chain of the class I HLA showed strongly different proximities to the IL-2R alpha, HLA-DR and ICAM-1 molecules, indicating that their orientations relative to the other proteins are dissimilar. IL-2R alpha molecules of the HUT-102B2 (T) cells are located mostly in the vicinity of the beta 2-microglobulin. In contrast, the local density of HLA-DR antigens is higher in the proximity of the heavy chain than in the vicinity of the beta 2-microglobulin. The possible functional significance of these protein patterns is also discussed herein.

Antibodies, Monoclonal↗
PubMed1987

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.

Arthritis↗
PubMed2004

[Alleles of HLA class II DRB1 of patients with essential hypertension in Yunnan Hans].

OBJECTIVE: To investigate the association between the alleles of human leukocyte antigens (HLA)-DRB1 and essential hypertension (EH) in the Hans living in Yunnan of China. METHODS: The alleles of HLA-DRB1 were typed by polymerase chain reaction-sequence specific primers (PCR-SSP) technique in samples from 83 patients with essential hypertension and 91 healthy controls. All of the subjects, their grandparents and grand-grandparents are Hans living in Yunnan of China. RESULTS: The frequency of DRB1*1501/2 in the EH patients (0.219) was significantly higher than that in the controls(0.060), chi quare=18.331, P<0.01. Relative risk (RR) was 4.46, and etiologic factor (EF) was 0.34. The frequency of DRB1*0901 significantly decreased in the group of patients with EH in comparison to the controls (0.081 versus 0.192) chi-square=8.704 P<0.05. RR was 0.41 and prevention factor(PF) was 0.19. CONCLUSION: HLA-DRB1*1501/2 is associated with the susceptibility to essential hypertension in the Yunnan Hans of China. DRB1*0901 may protect one from the disease.

Adult↗
PubMed1988

Generation of rabbit antipeptide antibodies to HLA-class II antigens by the use of synthetic peptides.

A group of eight synthetic peptides, corresponding in sequence to selected regions of HLA-DQ histocompatibility antigens, was used for rabbit immunization to examine their antigenicity and for localizing exposed regions in the native glycoproteins. Those antibodies were then tested in their ability to recognize the HLA-DQ alloantigens. Seven peptides elicited rabbit antibodies, four of which reacted with human glycoproteins prepared from chronic lymphocytic leukaemia cells. The results indicate that sequence stretches 63 to 79 and probably 82 to 93 of the beta chain correspond to exposed regions in DQw1, DQw2 and DQw3 molecules. However, the specificity of those antipeptide antibodies was low, due to extensive crossreactions with amino acid sequencies of high homology occurring in DQ alloantigens.

Amino Acid Sequence↗
PubMedDate not supplied

Expression of HLA class II in colorectal cancer: evidence for enhanced immunogenicity of microsatellite-instability-positive tumours.

Microsatellite-instability-positive (MSI+) colorectal cancers are characterised by an accumulation of deletion and insertion mutations at simple repeated sequences caused by inactivation of mismatch repair proteins. They share several clinicopathological features, including a better prognosis and a pronounced stromal inflammatory reaction. We have used suppression subtraction hybridisation between normal colonic epithelium and paired carcinomas to generate differential gene expression profiles in MSI+ and MSI- tumours. Following reverse northern blotting analysis, 11 genes were found to be up-regulated in the MSI+ tumour, and one of these specified the HLA-DM gene. This was in contrast to the MSI(-) tumour screen, where none of the clones analysed expressed this class of gene. Our results confirm that MSI(+) tumours may have a greater potential for the efficient presentation of antigens to the helper arm of the immune system and lend further support to the theory that the better prognosis of patients with MSI+ tumours may be linked to an enhanced immunogenicity of these tumours.

Base Sequence↗
PubMed1989

HLA class II restriction specificity of Dermatophagoides spp. reactive T lymphocyte clones that support IgE synthesis.

The results of recent experiments investigating the restriction specificity of cross-reactive, or Dermatophagoides farinae-specific, T cell clones isolated from an atopic individual with perennial rhinitis are reviewed. The restriction specificity was examined using serological inhibition, allogeneic presenting cells and murine fibroblasts expressing HLA-D region products. Although serological inhibition studies suggested that DR class II proteins were the major restriction elements used, the patterns of recognition observed with the allogeneic cell panel were complex, generally failing to correlate with the serologically defined MHC class II specificities. Analysis of the restriction patterns indicated that the majority of the T cell clones were restricted by DR beta III gene products and this was confirmed using murine fibroblasts expressing DRw52. DR beta I gene products functioned as restriction elements in the recognition of house dust mite allergen by the other clones. In an in-vitro model of allergen-dependent IgE synthesis, both DR beta I and DR beta III class II restricted T cells could be shown to provide functional help for IgE synthesized by autologous B cell-enriched populations.

Animals↗
PubMed1992

Susceptibility to IDDM in a Chinese population. Role of HLA class II alleles.

MHC associations with IDDM in a Chinese population were studied to investigate genetic susceptibility to the disorder. The frequency of HLA-DR3 was significantly higher in the diabetic patients (19/49 [38.7%] vs. control subjects, 11/105 [10.5%], Pc less than 1.3 x 10(-3), RR = 5.3 [CI 2.3-12.1]), whereas DR4 was not (11/49 [22.4%] vs. 28/105 [26.7%], NS). The frequency of DR3/4 heterozygosity was higher in the diabetic patients (6/49 [12.2%] vs. control subjects, 0/105 [0%], P = 1.7 x 10(-3), RR = 31.5 [CI 3.8-263.6]). The frequency of DR3/9 heterozygosity also was higher in the diabetic patients (6/49 [12.2%] vs. control subjects, 2/105 [1.9%], P = 0.03, RR = 6.2 [CI 3.0-12.7]). No significant associations were noted between DQB1 alleles and IDDM. Among DR4-positive subjects, the frequency of DQB1 allele DQB1*0302 was higher in the diabetic patients (10/11 [90.0%] vs. control subjects, 12/24 [50%], Pc less than 0.05, RR = 7.0 [CI 1.3-38.0]), and the frequency of DQB1*0401 was significantly lower in the diabetic patients (2/11 [18.2%] vs. control subjects, 16/24 [66.7%], Pc = 0.04, RR = 0.1 [CI 0.02-0.46]). No DR4 subtype was associated significantly with IDDM. The frequency of DQA1*0501, a DQA1 allele, was higher in diabetic patients (22/41 [53.7%] vs. control subjects, 20/95 [21.1%], Pc less than 3 x 10(-3), RR = 4.3 [CI 2.0-9.3]). The frequency of DQA1*0301, which has been associated consistently with IDDM in other ethnic groups, was not significantly higher in the diabetic patients in this study (27/41 [65.9%] vs. control subjects, 53/95 [55.8%], NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗