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PubMed1993

Cell action mechanism of tranilast--effect on the expression of HLA-class II antigen.

We tested the effect of Tranilast [N-(3',4'-dimethoxycinnamoyl anthranilic acid)], one of the anti-allergic agents, on the induction of interleukin 2 (IL2) responsiveness of lymphocytes from patients with bronchial asthma or hen-egg allergy following stimulation with Dermatophagoides farinae (Df) or ovalbumin (OVA), respectively. Mononuclear cells pretreated with Tranilast for 12 h failed to respond to IL2 following incubation with Df or OVA. Also Tranilast inhibited purified protein derivative (PPD)-induced IL2 responsiveness of normal lymphocytes but not the Con A-induced IL2 responsiveness of normal or allergen-sensitized lymphocytes. These results suggested that Tranilast has some immunosuppressive effect in that it inhibits antigen-induced IL2 responsiveness. Separation of potential target cells of Tranilast disclosed that antigen-presenting adherent cells were more susceptible to Tranilast than IL2-responding T-cell rich populations. Expression of HLA-DR and -DQ antigens but not DP antigens on macrophages, was significantly suppressed by treatment with Tranilast, although Tranilast scarcely decreased HLA class II antigens expression on B-cells. The suppression was overcome by interferon-gamma, which was known as an inducer for class II antigen expression. Taken together, Tranilast may suppress antigen-induced IL2 responsiveness by inhibiting HLA-DR and HLA-DQ antigens on macrophages.

Adult↗
PubMed2004

Is HLA class II susceptibility to primary antiphospholipid syndrome different from susceptibility to secondary antiphospholipid syndrome?

To assess whether the major histocompatibility complex (MHC) profile of patients presenting with primary antiphospholipid syndrome (PAPS) is different from that of patients with secondary antiphospholipid syndrome (SAPS), we studied 123 patients, 34 of whom presented PAPS and 35 SAPS due to systemic lupus erythematosus (SLE), 54 SLE patients without antiphospholipid syndrome (APS), and 166 controls. HLA-DRB1 and DQB1 alleles were typed using amplified DNA hybridized with sequence-specific primers. Compared to controls, PAPS patients exhibited a nonsignificantly increased frequency of DR53-associated alleles, and SAPS patients presented an increased frequency of HLA-DRB1*03 alleles (corrected P = 0.05). In addition, HLA-DRB1*03 alleles were over-represented in SAPS patients presenting anticardiolipin antibody (aCL) (Pc = 0.02), in SLE patients as a whole (Pc < 0.0001), and in SLE patients without APS (Pc = 0.02). The frequency of aCL among SLE patients presenting or not HLA-DRB1*03 alleles was closely similar. A trend to an increase in the frequency of the DQB1*0604 allele (14.3 versus 4.2%, P = 0.03) and of the DQB1*0302 allele (31.4 versus 12.7%, P = 0.01) was observed in SAPS. Taken together, these results indicate that the association of SAPS with HLA-DRB1*03 is due to the association with SLE and is not due to aCL, and suggest that the HLA class II profile of PAPS is different from that of SAPS.

Adolescent↗
PubMed2004

Down-regulation of HLA class II and costimulatory CD86/B7-2 on circulating monocytes from melanoma patients.

Antigen-presenting cells are crucial for the induction of an antigen-specific antitumoral immune response. Deteriorations in the expression pattern of cell surface molecules important for the presentation of antigens might therefore be indicative of an impaired immune response status in cancer patients. In the present study we investigated the expression of MHC class I and class II molecules, of the costimulatory molecules CD80/B7-1 and CD86/B7-2, of the adhesion molecule CD11c, and of the marker of activation CD71 on CD14+ peripheral blood monocytes (PBMs) from 144 melanoma patients in different stages of disease and 43 healthy controls, by flow cytometric analysis. We found a decreased expression of HLA-DR (p<0.0005), HLA-DQ (p=0.006), HLA-DP (p<0.0005), and CD86/B7-2 (p=0.001) on PBMs from melanoma patients compared with healthy controls, whereas no significant difference could be detected in the expression of HLA class I antigens and CD80/B7-1. This down-regulated expression was associated with disease progression. In contrast, CD71 expression was stage-dependently increased on PBMs from melanoma patients compared with healthy controls (p=0.024). No correlation was found between the PBM surface expression pattern and age, gender, tumor load, and current mode of therapy of the patients. The observed down-regulation of HLA class II and CD86/B7-2 on melanoma patients' PBMs might reflect an ineffective antigen-presenting function contributing to an impaired antigen-specific immune response in these patients.

Antigens, CD↗
PubMed2005

Mapping of immune responses following wild-type and mutant ABeta42 plasmid or peptide vaccination in different mouse haplotypes and HLA Class II transgenic mice.

Although the recent clinical trial of the ABeta42 peptide vaccine against Alzheimer's Disease (AD) has been halted due to adverse events, the apparent clinical utility of this approach underscores the need to further improve the safety of the vaccine, as well as to understand the potential immunological basis for complications. In this study, we examine both humoral and cellular immune responses elicited by immunization with peptide or DNA encoding wild-type and the Flemish and Dutch mutations of ABeta42 (i.e. the beta amyloid peptide spanning amino acids 1-42) in mice of different immune haplotypes as well as HLA Class II transgenic mice. The Flemish and Dutch mutations have been associated with cerebrovascular hemorrhages in affected individuals. These data allow determination of potential immunological responses that could mediate pathology observed with mutant forms of amyloid beta, as well as lead to the generation of safer vaccine preparations. Following peptide or plasmid immunization, antibody responses were measured against the different ABeta42 peptides in an ELISA assay, while T cell epitopes were analyzed through interferon gamma ELISPOT and lymphocyte proliferation assays. B cell mapping studies indicated that sera from all of the haplotype mice vaccinated with any of the ABeta42 peptides reacted specifically to the first 10 amino acids of ABeta42 with the ABeta42 mutants eliciting higher immune responses. ELISPOT analysis, which accessed cellular immune responses indicated that mice expressed differences in Class I epitopes dependent on the different immune haplotypes. These results may have implications for the design of future ABeta42 based vaccines against Alzheimer's Disease.

Amino Acid Sequence↗
PubMed1987

A novel HLA class II alloantigen detected by an alloantiserum TK2.

An alloantiserum, TK2, obtained from a kidney transplant patient, was investigated. TK2 reacted with B lymphocytes that had only one detectable DQ antigen. DQ "blank" homozygous cell lines were positive for TK2, but DQwl, DQw2, and DQw3 homozygous cell lines failed to react with TK2. Positive reactions for TK2 segregated with DQ "blank" haplotypes in the families studied. The reactivity of TK2 to B lymphocytes was strong, while its reactivity to monocytes was very weak. When TK2 was absorbed with DQ "blank" cells, it became unreactive to other lymphocytes. TK2 blocked the binding of an anti-DQ monoclonal antibody to DQ "blank" cells. It did not affect the binding of the antibody to DQw1 and DQw3 cells, nor did it affect the binding of an anti-DR monoclonal antibody to a DQ "blank" cell line. These findings suggest that TK2 can detect a new HLA class II alloantigen that corresponds to a DQ "blank" specificity.

Antibodies, Monoclonal↗
PubMed2000

Extensive genetic alterations of the HLA region, including homozygous deletions of HLA class II genes in B-cell lymphomas arising in immune-privileged sites.

In B-cell lymphomas, loss of human leukocyte antigen (HLA) class I and II molecules might contribute to immune escape from CD8(+) and CD4(+) cytotoxic T cells, especially because B cells can present their own idiotype. Loss of HLA expression and the possible underlying genomic alterations were studied in 28 testicular, 11 central nervous system, and 21 nodal diffuse large B-cell lymphomas (DLCLs), the first two sites are considered as immune-privileged sites. The analysis included immunohistochemistry, loss of heterozygosity analysis, and fluorescent in situ hybridization (FISH) on interphase cells and isolated DNA fibers. Total loss of HLA-A expression was found in 60% of the extranodal cases and in 10% of the nodal cases (P <.01), whereas loss of HLA-DR expression was found in 56% and 5%, respectively (P <.01). This was accompanied by extensive loss of heterozygosity within the HLA region in the extranodal DLCLs. In 3 cases, retention of heterozygosity for D6S1666 in the class II region suggested a homozygous deletion. This finding was confirmed by interphase FISH that showed homozygous deletions in the class II genes in 11 of the 18 extranodal lymphomas but in none of the 7 nodal DLCLs (P <.001). Mapping by fiber FISH showed variable deletions that always included HLA-DQ and HLA-DR genes. Hemizygous deletions and mitotic recombinations often involving all HLA genes were found in 13 of 18 extranodal and 2 of 7 nodal lymphomas. In conclusion, a structural loss of HLA class I and II expression might help the B-cell lymphoma cells to escape from immune attack.

Adolescent↗
PubMed2004

A theoretical approach for T-lymphocyte monitoring of autologous cancer vaccine therapy using autologous HLA-class I and HLA-class II constructs.

It is desirable to have in vitro surrogate endpoints that reflect changes in cellular immunity in patients who are undergoing treatment with anticancer, autologous, tumor-cell vaccines. The tetramer assay appears to be useful for monitoring T-lymphocyte responses to a single, specific, known tumor peptide antigen, but cell-based vaccines may express multiple tumor-associated antigens that are important in a host immune response to their own cancer. We describe a hypothetical alternative to the standard artificial tetramer assay, that has the potential to detect CD4+ and CD8+ T-lymphocytes that react with any peptides expressed in the context of HLA-class I or HLA-class II. Such an assay should enable monitoring for specific T-lymphocyte antitumor activity in patients being treated with patient specific, autologous, tumor-cell vaccines.

Cancer Vaccines↗
PubMed1988

Identification of homologous regions in human immunodeficiency virus I gp41 and human MHC class II beta 1 domain. I. Monoclonal antibodies against the gp41-derived peptide and patients' sera react with native HLA class II antigens, suggesting a role for autoimmunity in the pathogenesis of acquired immune deficiency syndrome.

Homologous regions of five amino acids each, were identified in the NH2-terminal domain of human class II beta chains and the COOH terminus of HIV I envelope protein. The homologous regions are highly conserved among different DR and DQ alleles and also among different isolates of HIV. Septamers containing these sequences were synthesized and used for the generation of murine mAbs. The mAbs selected for this study were raised against the HIV I-derived peptide and reacted strongly not only with the immunizing peptide, but also with the homologous class II-derived peptide. These mAbs also reacted with native MHC class II antigens expressed on human B cell lines and on murine fibroblast L cell lines transfected with the genes coding for the alpha and beta chains of human class II antigens. Furthermore, sera from 36% of AIDS patients tested contained antibodies that reacted with the class II-derived peptide, as well as with intact class II molecule-rich cell extracts. Such antibodies in HIV I-infected individuals may recognize self class II antigens, triggering autoimmune mechanisms that could contribute to the development of immunodeficiency in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1988

HLA class II restriction specificity for nickel-reactive T lymphocytes.

Nickel-specific T cells were primed in vitro and restimulated with nickel in combination with autologous or allogeneic antigen-presenting cells. We have previously shown that not only DR, but also DQ molecules may take part in this process. To investigate this phenomenon further we applied recently available knowledge based on studies using specific cDNA probes and Restriction Fragment Length Polymorphism (RFLP), which has revealed a new level of DQ polymorphism, to search for a correlation of this polymorphism in the function of nickel-reactive T lymphocytes. We found that DQ, and presumably also DR, may restrict the proliferative response to nickel. The capacity of various antigen-presenting cells to cause restimulation correlated well, though not completely, with the specificity DQw1. RFLP splits of DQw1 did not yield any additional information on restriction specificity. Experiments using anti DR, DQ and DP monoclonal antibodies were performed, showing similar blocking capacity in all three antibodies. Work with cloned T cells is in progress to obtain more clearcut results concerning the HLA class II restriction of the proliferative T lymphocyte response to nickel.

Antigen-Presenting Cells↗
PubMed1989

Calcitriol inhibits the PHA-induced production of IL-2 and IFN-gamma and the proliferation of human peripheral blood leukocytes while enhancing the surface expression of HLA class II molecules.

1 alpha-dihydroxivitamin D3 [calcitriol; 1,25-(OH)2D3], the most biologically active metabolite of vitamin D3, exerts several effects on peripheral blood mononuclear cells (PBMC). We report here the effects of calcitriol on PBMC proliferation and on the expression of some lymphocyte surface differentiation markers, as well as its action on lymphokine production. Calcitriol inhibited the proliferation of PHA-activated PBMC in a dose-dependent manner, with peak activity at 10(-8) M. Exposure of PHA-stimulated PBMC to 10(-8) M calcitriol for 3 days tended to increase the percent of CD4- and CD8-positive cells, though statistical significance was not reached. A more striking effect of calcitriol was seen on the expression of the non-polymorphic determinants of HLA class II DR molecules; in cultures stimulated with PHA for 3 or 4 days; 10(-8) calcitriol doubled the percent of DR-positive cells as compared to controls treated with PHA alone. This activity peaked at 10(-9) M, a supra-physiologic dose. After 3 days in culture, 10(-8) M calcitriol strongly inhibited the production of both IL-2 and IFN-gamma. This effect was evident at different PHA concentrations (0.5, 1.5 and 3.0 micrograms/ml), and almost disappeared at 10(-10) M. These results underline the immunoregulatory role of calcitriol, but well defined experimental models in vitro are needed for elucidating the relevance of this compound in physiology and, possibly, in therapeutics.

Antigens, Differentiation↗
PubMed2003

Mycobacterium bovis BCG scar status and HLA class II alleles influence purified protein derivative-specific T-cell receptor V beta expression in pulmonary tuberculosis patients from southern India.

Purified protein derivative (PPD) RT23-recalled T-cell receptor (TCR) V beta expression was studied in the peripheral blood of 42 pulmonary tuberculosis patients and 44 healthy controls from southern India, a region where tuberculosis is endemic. Forty-eight-hour whole-blood cultures in the presence or absence of PPD-RT23 were set up, and at the end of the culture period total RNA was extracted and cDNA was synthesized. Expression of various TCR V beta families was assessed by using family-specific primers. PPD-specific expression (usage) of TCR V beta families 4, 6, 8 to 12, and 14 was found in more controls than patients. Among the responders (individuals who showed PPD-specific expression), endemic controls had significantly higher responses than the patients had for TCR V beta families 2, 3, 7, 13, and 17. The majority of the patients did not show usage of most of the TCR V beta families, and this was attributed to T-cell downregulation. A four-way nested classification analysis revealed that TCR V beta family 1, 5, 9, 12, and 13 usage in the context of HLA class II high-risk alleles (DRB1*1501, DRB1*08, and DQB1*0601) and Mycobacterium bovis BCG scar status were the determining factors in susceptibility and resistance to tuberculosis. The healthier status of controls was attributed to the wider usage of many TCR V beta families readily recalled by PPD, while the disease status of the patients was attributed to TCR V beta downregulation and the resultant T-cell (memory cell?) unresponsiveness. Host genetics (HLA status) and BCG vaccination (scar status) seem to play important roles in skewing the immune response in adult susceptibility to pulmonary tuberculosis through TCR V beta usage.

Adult↗
PubMed1999

HLA class II restriction of autoreactive T cell responses in pemphigus vulgaris: review of the literature and potential applications for the development of a specific immunotherapy.

Pemphigus vulgaris (PV) is a life-threatening autoimmune bullous disease of the skin and mucous membranes which requires immunosuppressive therapy, most commonly a combination of glucocorticoids and additional immunosuppressive agents. Since the side effects of long-term immunosuppressive therapy contribute to the poor prognosis of this disorder, there is considerable interest in a more specific treatment of this severe skin disease. PV may serve as a model disease for the development of a specific immunotherapy, because its pathogenesis as well as involved immunogenetic factors are well-characterized. This review focuses on the characterization of autoreactive T cell responses to desmoglein 3 (Dsg3), the autoantigen of PV, that presumably regulate the production of autoantibodies by providing help to the autoreactive B cells. Current knowledge on T cell epitopes of Dsg3 and the HLA class II alleles that restrict Dsg3-specific autoreactive T cell responses, as well as potential applications for a specific immunotherapy of PV, are described.

Amino Acid Sequence↗
PubMed1996

A structural model for TCR recognition of the HLA class II shared epitope sequence implicated in susceptibility to rheumatoid arthritis.

HLA molecules associated with rheumatoid arthritis (RA) contain a discrete structural element known as the shared epitope, a set of conserved amino acid residues located on the alpha helical portion of the class II beta chain. Each of the different HLA molecules associated with RA contain the same shared epitope sequence, although they may vary markedly in other regions of the class II structure, which also determine peptide-class II interactions. Previous mutagenesis studies and structural modelling indicate that key polymorphic amino acid side chains within the shared epitope sequence are in locations likely to contact the T cell receptor (TCR) during the trimolecular activation reaction between the HLA-peptide complex and TCR. We have evaluated the potential structural basis for such shared epitope recognition by analysing detailed molecular models of the arthritis-associated DRB1*0404 molecule and a T cell receptor from T cell clone EM025, specific for HLA-DR4 molecules which carry the shared epitope. A likely orientation for the trimolecular complex was deduced in which the EM025 alpha chain interacts with the DR alpha chain and the EM025 beta chain interacts with the DR beta chain; residues Q70 and R71 within the DR beta chain shared epitope region are positioned for hydrogen bond interactions directly with Q97 of the TCR beta CDR3 region, D30 of the TCR beta CDR1 region, and possibly N51 of the TCR beta CDR2 region, indicating a degree of specific selection and interaction which encompasses multiple TCR contacts. These findings suggest a structural basis for the genetic associations with the HLA shared epitope and the potential contribution of this region to oligoclonal T cell selection and expansion in RA.

Arthritis, Rheumatoid↗
PubMed1989

Activation of human T cells by toxic shock syndrome toxin-1: the toxin-binding structures expressed on human lymphoid cells acting as accessory cells are HLA class II molecules.

Toxic shock syndrome toxin-1 (TSST-1)-binding assay using 125I-labeled TSST-1 showed the presence of specific TSST-1 binding in a B cell fraction of human peripheral blood mononuclear cells and L cells transfected with DR2 genes or DR4 genes but not in a T cell fraction and control L cells. Fixation with paraformaldehyde, an inhibitor of antigen processing, did not remove TSST-1-binding activity of the transfectants. Binding of 125I-labeled TSST-1 to the transfectants was reduced by an anti-DR monoclonal antibody. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed the presence of a single band with TSST-1-binding activity and the same migration pattern as DR heterodimers. TSST-1-induced T cell responses, proliferation and interleukin 2 (IL2) production were observed in the presence of the transfectants but not in the presence of control L cells, while concanavalin A-induced IL2 production was observed in the presence of either the transfectants or control L cells. Presence of an anti-DR monoclonal antibody inhibited the TSST-1-induced responses. Paraformaldehyde-fixed Daudi cells were effective in supporting TSST-1-induced IL2 production by T cells. These results indicate that HLA class II molecules directly bind intact TSST-1 and perform an essential role as the TSST-1-binding structures on accessory cells in T cell activation by the toxin.

Antigen-Presenting Cells↗
PubMed1995

The presence of the HLA class II allele DPB1*0501 in ethnic Thais correlates with an enhanced vaccine-induced antibody response to a malaria sporozoite antigen.

In this study, we examined the correlation between the frequency of allelic variants of the class II human leukocyte antigen (HLA) DR, DQ and DP gene loci and the quantitative humoral immune response observed in 71 Thai volunteers, subsequent to vaccination with a conjugated subunit vaccine. This vaccine was designed to induce antibodies directed against the immunodominant repeat region of the Plasmodium falciparum circumsporozoite (CS) protein. The presence of the DPB1*0501, a relatively common allele in Asian populations, was found to be associated with high vaccine-induced CS repeat-specific antibody responses in the volunteers. Given the increasing focus on the use of subunit vaccines in the control of infectious diseases, consideration of the influence of class II allele frequencies in ethnically diverse recipient populations may be important.

Adult↗
PubMed1997

Quality control for DNA contamination in laboratories using PCR-based class II HLA typing methods.

Quality control (QC) in laboratories performing molecular histocompatibility class II typing often includes a polymerase chain reaction (PCR) approach for monitoring DNA contamination. An oligonucleotide primer set was designed, (RBQBf/RBQBr), which is specific for nonpolymorphic regions of the DR-B, DQ-B, and DP-B consensus sequences with an expected PCR product size of 81 bp. RBQBf/RBQBr detected genomic DNA from reference cell lines LWAGS and BM21 (50 to 100 picograms) as well as DR-B, DP-B, and DQ-B amplicon (1 copy). Additionally, RBQBf/RBQBr detected SSP products from routine DR-B and DQ-B typings. Validation studies employing controlled DNA contamination of laboratory surfaces revealed that increasing amounts of wipe test samples (5% to 20% v/v) were inhibitory to the wipe test PCR, whereas lower amounts (1% to 2%), or alternatively, a diluted wipe test sample, increased the sensitivity of the test and optimized the results. Collectively, this study describes a primer set, RBQBf/RBQBr, which detects both genomic DNA and DR-B, DQ-B, or DP-B amplicon and furthermore illustrates the necessity of routine testing for potential inhibitory factors that may be introduced into the wipe test PCR.

Base Sequence↗
PubMed2005

Different contribution of class II HLA in fulminant and typical autoimmune type 1 diabetes mellitus.

AIMS/HYPOTHESIS: Fulminant type 1 diabetes, which is characterised by a markedly acute onset of diabetes and an absence of islet-related autoantibodies, accounts for 20% of type 1 diabetes in Japan. We aimed to clarify the contribution of the HLA subtype to fulminant type 1 diabetes in Japanese. METHODS: We determined the serological subtypes of HLA-A, -DR and -DQ in 115 patients with fulminant type 1 diabetes, 98 patients with typical type 1A diabetes and 190 normal control subjects. RESULTS: The frequency of HLA-DR4, but not DR9, was significantly higher in fulminant type 1 diabetes, while those of HLA-DR1, DR2, DR5 and DR8 were significantly lower than those in controls. In contrast, DR9 but not DR4 was more frequent and DR2 was extremely rare in typical type 1A diabetes. Haplotype analysis revealed that DR4-DQ4 was significantly more frequent, and both DR2-DQ1 and DR8-DQ1 were less frequent in fulminant diabetes. In type 1A diabetes, DR2-DQ1 was extremely rare while DR9-DQ3 was significantly more frequent. In the combination analysis, the homozygotes of DR4-DQ4 in fulminant type 1 diabetes and DR9-DQ3 in typical type 1A diabetes indicated high odds ratios (13.3 and 13.3, respectively). CONCLUSIONS/INTERPRETATION: Our results suggest that class II HLA contributes to the development of fulminant type 1 diabetes. Susceptibility and resistance of the HLA subtype to type 1 diabetes are distinct between fulminant and typical autoimmune type 1 diabetes.

Adolescent↗
PubMed2003

HLA expression and immunologic properties of differentiated and undifferentiated mesenchymal stem cells.

OBJECTIVE: Mesenchymal stem cells (MSC) do not elicit alloreactive lymphocyte responses due to immune modulations. We investigated the immunologic properties of MSC after differentiation along three lineages: bone, cartilage, and adipose. METHODS AND RESULTS: Flow cytometry showed that undifferentiated MSC express HLA class I but not class II, although HLA class II was present intracellularly as detected by Western blot. Addition of interferon gamma (IFN-gamma) for 48 hours induced greater than 90% of cells to express HLA class II. No lymphocyte response was induced by allogeneic irradiated MSC as stimulators. Results were similar using MSC pretreated with IFN-gamma. After growth of cells in medium to induce differentiation to bone, cartilage, or adipose for 6 or 12 days, the expression of HLA class I increased but no class II was detected on the cell surface. The ability to upregulate HLA class II on the cell surface after exposure to IFN-gamma for 48 hours was clearly diminished after the cells had been cultured in differentiation medium for 6 or 12 days, with only 10% of cells expressing HLA class II. Using MSC grown in osteogenic, chondrogenic, or adipogenic medium as stimulator cells, no lymphocyte alloreactivity was seen, even if differentiated MSC had been pretreated with IFN-gamma. MSC inhibit mixed lymphocyte cultures, particularly after osteogenic differentiation. This suppression was further enhanced by IFN-gamma. CONCLUSIONS: Undifferentiated and differentiated MSC do not elicit alloreactive lymphocyte proliferative responses and modulate immune responses. The findings support that MSC can be transplantable between HLA-incompatible individuals.

Adolescent↗