Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HLA class II”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1994

HLA class II genes in Vogt-Koyanagi-Harada disease.

PURPOSE: Vogt-Koyanagi-Harada disease (VKH) is an autoimmune disorder causing a bilateral diffuse granulomatous uveitis, often with several associated extraocular manifestations. Strong association of human leukocyte antigens (HLA) antigens with the disease has been documented. The details of all HLA class II genotypes were investigated in Japanese patients with VKH to demonstrate the immunogenetic background of the disease. METHODS: Human leukocyte antigen tissue typing was performed in 57 Japanese patients with VKH by the modified two-stage complement-dependent microcytotoxicity method. DNA analyses were done by polymerase chain reaction (PCR)-single-strand conformation polymorphism and PCR-restriction fragment-length polymorphism methods. RESULTS: The frequencies of HLA-DR4 and HLA-DQ4 were 93% and 83% among the patients with VKH, compared with 43% and 32% among the controls, respectively (relative risks, 17.4 and 9.9; Pc < 1.0 x 10(-10)). At the genomic level, all patients had the HLA-DQA1*0301 genotype, which was present in only 67% of the normal controls (relative risk, 56.5; Pc < 1.0 x 10(-5)). With allelic combinations, -DQA1*0301/-DR4 showed the greatest relative risk ratio. Conversely, DQB1*0604 genotype was not detected among the patients. CONCLUSION: It can be postulated that VKH is a disease of combined allelic predisposition in which DQA1*0301 acts as the primary and HLA-DR4 acts as an additive factor in the development of the disease. Based on the negative association of DQB1*0604, we propose that DQB1*0604 provides considerable protection, possibly by altering other factors in the pathogenesis of VKH in the Japanese.

Base Sequence↗
PubMed1999

Small bowel T cells, HLA class II antigen DR, and GroEL stress protein in IgA nephropathy.

BACKGROUND: Previous studies suggest that intestinal mucosa may be involved in the pathogenesis of IgA nephropathy (IgAN). To further clarify this involvement, we investigated whether or not IgAN patients have small bowel mucosal findings suggestive of inflammation and stress. METHODS: Seventeen patients with IgAN underwent gastroscopic examination. Fresh small bowel biopsy specimens were frozen, and in cryosections, the proportion of alphabeta and gammadelta receptors bearing T cells and CD3+ T cells were quantitated immunohistochemically. The expression of HLA class II antigen DR (HLA-DR) and human GroEL stress-protein homologue was similarly quantitated. In an avidin-biotin peroxidase technique, the following monoclonal primary antibodies were used: anti-beta-chain (betaF1), anti-delta-chain (TCRdelta1), anti-CD3 (Leu4), anti-constant fragment of HLA-DR (L243), and anti-GroEL (ML30). Twenty-nine patients who had undergone gastroscopy because of dyspepsia served as controls. RESULTS: In all specimens, the mucosal architecture was normal. The amount of gammadelta T cells and the total amount of T cells, as indicated by CD3+ positivity, were both significantly increased in IgAN. The number of alphabeta T cells was also higher in the IgAN patients. Villous epithelium of the IgAN patients disclosed a significant increase in the expression of HLA-DR antigen and GroEL stress protein. CONCLUSIONS: Our results suggest that ongoing small bowel inflammation and stress are present in IgAN. Despite normal morphology, there is reason to believe that the small bowel mucosa is involved in the pathogenesis of IgAN.

Adult↗
PubMed1998

The CLIP-substituted invariant chain efficiently targets an antigenic peptide to HLA class II pathway in L cells.

The presentation of antigenic peptides by major histocompatibility complex (MHC) class II to CD4+ T cells is crucial to initiate immune responses. We developed a new system for delivery of an antigenic peptide to the MHC class II pathway, using the invariant chain (Ii). We designed a mutated human p33-form Ii, CLIP-substituted Ii, in which streptococcal M12p55-68 (RDLEQAYNELSGEA) was substituted for CLIP (class II associated invariant chain peptide). We examined the peptide presenting function of this construct, in comparison with the previously reported C-terminal fused Ii, in which a cathepsin cleavage site and M12p54-68 was ligated to the C-terminus of Ii. Mouse L cell transfectants expressing either of these two mutated Ii along with HLA-DR4 could process and present M12p55-68 to the peptide specific and DR4-restricted CD4+ T cell clone. CLIP-substituted Ii was much more efficient in antigen presentation than was the C-terminal fused Ii. Similar to the wild-type Ii, the CLIP-substituted Ii was associated intracellularly with DR4 molecules. These results indicate that the peptide substituted for CLIP of Ii p33 bound to the groove of DR molecules in the same manner as CLIP and it was preferentially presented to the CD4+ T cell clone in the absence of HLA-DM molecules. This system may prove useful for immunotherapy with DNA vaccines or for construction of an antigen presenting cell library with diverse peptides.

Amino Acid Sequence↗
PubMed1999

Association of HLA class II alleles with different subgroups of diabetes mellitus in Eastern India identify different associations with IDDM and malnutrition-related diabetes.

Genetic studies of Malnutrition related diabetes are few. We have analyzed HLA class II gene polymorphism in different types of diabetes mellitus patients from Cuttack in Eastern India. Patients with insulin-dependent diabetes mellitus (IDDM), non-insulin-dependent diabetes mellitus (NIDDM) and malnutrition-related diabetes mellitus (MRDM), which is subdivided into protein-deficient diabetes mellitus (PDDM) and fibrocalculous pancreatic diabetes (FCPD), were studied and their associations with autoantibody markers. IDDM and PDDM were associated with DR3 and DQ2 but not DR4 and DQ8. FCPD was positively associated with DQ9 (A*0201-B*0303). The association of DQ9 with FCPD suggests differences in the genetic background for susceptibility between IDDM and MRDM in the Cuttack population. There is no association seen between HLA-DR-DQ and NIDDM patients from Eastern India. Clinical classification of diabetes into IDDM, NIDDM and MRDM does not identify the underlying pathological mechanisms. Presence of autoantibodies to IDDM autoantigens in clinical MRDM and NIDDM identifies the slow-onset form of IDDM. Due to the absence of autoantibody assays for diagnosis of IDDM in India, slow onset IDDM is not diagnosed and the patients are classified as NIDDM or MRDM. Our study demonstrates that the presence of GAD65 antibody and DR3-DQ2 positivity in MRDM and NIDDM patients in Eastern India would suggest the presence of slow-onset IDDM. Our data would indicate alternatively that MRDM can coexist with IDDM in these patients and malnutrition could be one of the reasons for the slower onset in IDDM-prone individuals.

Alleles↗
PubMed1993

Rapid DNA typing for class II HLA antigens: subtyping of DRw52-associated DRB1 alleles.

Serologic typing for MHC class II antigens is incapable of identifying important subtypes for certain DRB1 alleles and occasionally leads to errors of assignment, particularly with the DR antigens associated with DRw52. To simplify DNA typing of DRw52-associated DRB1 alleles, we have developed a new rapid method using PCR-RFLP. The PCR-RFLP method is based on allele-specific amplification followed by digestion of PCR-amplified DNA with restriction enzymes. Group-specific amplification of the second exon of DR3, DR5, DR6 and DR8 was achieved using a 5' primer specific for the first hypervariable region sequence common to all alleles in this group and generic 3' primers. Human genomic DNA was amplified in a Perkin-Elmer Thermocycler. The presence of a 265 bp fragment was confirmed by agarose gel electrophoresis. Restriction enzyme digestion using Rsa I followed by polyacrylamide gel electrophoresis gave a pattern unique for some alleles and placed the remainder in subgroups. Digestion of the PCR product with one or two of the following enzymes (Asp 700, Hae II, Mnl I, Mbo II, Ksp I and Hph I) permitted the identification of 21 of the 22 alleles. DRB1*1103 and DRB1*1104 are not distinguished by this method and can be distinguished by SSOP or by using a specific 3' primer. For some heterozygous combinations, additional primers are used to provide full subtyping. This method provides a rapid and less costly alternative to PCR-SSOP for DRw52 subtyping in the smaller laboratory as only one amplification is required (two primers) for the majority of samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1989

Restriction fragment length polymorphism analysis with a cross-reactive HLA class II DR-beta gene probe for the detection of engraftment of MHC-mismatched marrow in the rhesus monkey.

Our interest in MHC-mismatched allogeneic bone marrow transplantation (BMT) in the rhesus monkey prompted us to investigate restriction fragment length polymorphism analysis as a means for detecting lymphohematopoietic chimerism in the primate. A human MHC (HLA) class II DR beta gene cDNA probe was tested on rhesus peripheral blood mononuclear cell DNA digested with any of three restriction enzymes. We found that (1) the human DR beta probe hybridized to as many as 15 restriction fragments per rhesus DNA sample, suggesting cross-hybridization at more than one locus of rhesus MHC class II beta genes; (2) restriction fragment length polymorphisms were common among outbred monkeys as a result of class II beta gene polymorphisms and would be sufficient for chimerism detection in the majority of random pairs of outbred monkeys utilizing only a single restriction enzyme (Bgl II); and (3) sensitivity (5-10% chimerism) was comparable to that reported for restriction fragment length polymorphism assays utilizing non-MHC probes in clinical HLA-identical BMT. Utility of the assay was demonstrated in a preliminary series of experiments in rhesus monkeys conditioned with mixed T cell-depleted MHC-mismatched allogeneic plus T cell-depleted autologous BMT with or without cardiac allograft implantation.

Animals↗
PubMed2002

Epistasis between DSG1 and HLA class II genes in pemphigus foliaceus.

Pemphigus foliaceus (PF) is a rare and severe cutaneous autoimmune disease caused by autoantibodies directed against desmoglein 1 (DSG1), a desmosomal adhesion glycoprotein. We previously showed that the DSG1 gene is polymorphic and that a coding synonymous T/C single nucleotide polymorphism at position 809 is associated with PF. To determine whether the disease occurred as a consequence of complex genetic interactions, we simultaneously examined the contribution of major histocompatibility complex (MHC) class II and DSG1 polymorphisms to PF susceptibility. Our analysis performed in 31 PF patients and 84 healthy controls first confirmed the previously reported common DRB1*04 and DRB1*14 genetic background in PF and individualized DRB1*0102, DRB1*0402 and DRB1*0406, and DRB1*1404 as susceptibility MHC class II alleles in French Caucasian PF patients. It also showed that the C/C(809) genotype was associated with PF. Combined analysis of HLA class II and DSG1 polymorphisms with several distinct statistical methods including logistic regression, showed that the DRB1*04 allele and the C/C(809) genotype interact to confer a higher susceptibility to PF. These data demonstrate the role of epistasis between individual genes in PF susceptibility and illustrate the genetic complexity of organ-specific autoimmune diseases.

Autoantigens↗
PubMed2000

HLA class II DRB1, DQB1, DPB1 polymorphism and cardiomyopathy due to Trypanosoma cruzi chronic infection.

Trypanosomiasis is an important cause of cardiomyopathy in endemic rural areas of Latin America. Previous studies have suggested participation of HLA molecules in the immune response regulation of T. cruzi infection, and association of HLA antigens with heart damage. One hundred and eleven unrelated T. cruzi antigen-seropositive individuals were tested for HLA class II alleles by the polymerase chain reaction and sequence specific oligonucleotide (PCR-SSO) method. Patients were classified in 3 groups according to clinical and electrocardiographic characteristics: asymptomatics (group A), with arrhythmia (group B), and with overt congestive heart failure (group C). Statistical analysis confirmed the significant increment of the DRB1*01 DQB1*0501 haplotype (p = 0.03) previously reported by our laboratory in patients with cardiomyopathy. The DPB1*0401 allele frequency is also significantly increased in patients with heart disease (groups B + C) (p = 0.009) while DPB1*0101 frequency is higher among the asymptomatic group (p = 0.04) compared with individuals of group C. The DPB1*0401 allele in homozygous form or in combination with allele DPB1*2301 or 3901, was found present more often in patients of groups B and C. Thus, the combination of two of these three alleles, sharing specific sequence motifs in positions 8, 9, 76, and 84-87 confers a relative risk of 6.55 to develop cardiomyopathy in seropositive patients (p = 0.041). Furthermore, 32% of the cardiomyopathics have either DRB1*01 DQB1*0501 and/or DPB1*0401/*0401, 0401/*2301, or* 0401/*3901 compared with 9% of the seropositive asymptomatics (OR = 5.0; p = 0.006).

Amino Acid Sequence↗
PubMed1988

Occurrence of thyrocyte HLA class II expression in a wide variety of thyroid diseases: relationship with lymphocytic infiltration and thyroid autoantibodies.

The proteins of the major histocompatibility system (HLA in humans) play an essential role in the regulation of immune responses due to their involvement in the presentation of antigen to T lymphocytes. Thyroid follicular cells (thyrocytes) from patients with Graves' disease and Hashimoto's thyroiditis demonstrate increased expression of HLA class I and aberrantly or inappropriately express class II antigens, a phenomenon that may play an important role in the pathogenesis of these autoimmune diseases. To establish if these changes in the expression of HLA molecules are characteristic of thyroid autoimmune disease, the immunopathological features (including class I and class II antigen expression) of 100 thyroidectomy specimens from patients with nonautoimmune thyroid disease were studied by indirect immunofluorescence, and the results compared with the findings in specimens from 14 patients with Graves' disease and 12 subjects undergoing laryngectomies for carcinoma. Increased class I product expression was found in 61% of all tissues studied, with maximal occurrence in papillary carcinomas (100%) and Graves' disease (86%), but it was also detected in 50% of the glands containing nodular lesions and in 16% of the control glands. Inappropriate class II molecule expression was found in Graves' disease (71%), hyperplastic nodules (53%), multinodular glands (44%), papillary carcinomas (38%), and 16% of the control glands. In summary, an increase in inappropriate HLA class I and class II expression was very common in nonautoimmune thyroid glands, but it generally occurred in the context of lymphocytic infiltration and thyroid autoantibodies (i.e. focal thyroiditis). Multiple correlation analyses of these 4 phenomena indicated heterogeneity in the mechanism leading to the inappropriate expression of thyrocyte class II antigens in the different conditions studied.

Adolescent↗
PubMed1997

HLA class II profile: a weak determinant of factor VIII inhibitor development in severe haemophilia A. UKHCDO Inhibitor Working Party.

The risk of developing factor VIII inhibitor antibodies in haemophilia A may relate both to factor VIII genotype and genes within the HLA complex known to influence immune response. We investigated a cohort of 176 patients with severe haemophilia A and with either high-level inhibitors (> 10BU/ml) or with no history of an inhibitor, stratified according to the presence or absence of the factor VIII gene intron 22 inversion. HLA DRB1, DQA1 and DQB1 polymorphisms were determined by PCR. HLA frequencies form 137 United Kingdom controls were used for comparison. HLA phenotype frequency differences, expressed as odds ratios with 95% confidence intervals were as follows: HLA-DRB*1501, DQB1*0602 and DQA1*0102 were all increased in frequency in patients with inhibitors, only DQA1*0102 reaching statistical significance (OR 2.7, 1.2-5.9). These alleles form part of an established HLA haplotype. The frequencies of HLA-DRB1*1501, DQB1*0602 and DQA1*0102 were particularly raised in patients with inhibitors and a factor VIII gene intron 22 inversion, although again only DQA1*0102 achieved significance (OR 3.1, 1.0-10.1). The frequency of DRB1*01, DQB1*0501, DQA1*0101 were also increased in inhibitor patients lacking the intron 22 inversion although this failed to achieve statistical significance. This data suggests that HLA class II profile constitutes a weak risk factor for developing inhibitor antibodies to factor VIII. This may be more pronounced in patients with an intron 22 inversion.

Chromosome Inversion↗
PubMed1993

[Cartilage transplantation in the area of the head-neck: comparative study of HLA class II antigen induction to chondrocytes in various culture systems].

Autologous and homologous cartilage grafts are often used in reconstructive head and neck surgery. Unfortunately, sometimes the outcome of such operations is endangered by graft rejection or resorption. Among other reasons, immunological reactions with HLA class II antigen expression are thought to be involved at least in failures of vitally grafted cartilage. Up to now, only one case of class II antigen expression in a cartilage graft "in vivo" has been reported. Nevertheless, it has already been demonstrated that stimulated cartilage cells are able to express "in vitro" class II antigens if grown in monolayer cultures. However, it has also repeatedly been shown that chondrocytes reveal strong dedifferentiating features if cultured in monolayers. Therefore, it was the aim of this study to examine whether isolated and stimulated chondrocytes also express class II antigens if cultured under in vitro conditions closer to the relevant in vivo situation. Hence monolayer, suspension, agar, alginate and organ cultures were prepared simultaneously and kept for up to 60 days. Chondrocytes were stimulated by the addition of IFN-gamma and tested for class II antigens. For the detection of the antigens immunocyto- and immunohistochemical APAAP stainings as well as flow cytometric measurements were made. In all examined culture systems a class II antigen induction could be observed. Any significant differences between the various cultures as to the intensity of antigen expression could not be detected. Consequently, the expression of class II antigens on stimulated human chondrocytes seems not to be a specificity of monolayer cultures. Therefore, class II antigen induction may be considered to play a role in the rejection/resorption of vitally grafted cartilage in reconstructive surgery.

Cartilage↗
PubMed2000

[A probe for evaluating the role of HLA class II antigens coded with the DRB gene in etiopathogenesis of familial sarcoidosis in Poland using the K-nearest neighbor experimental statistical method].

The aim of this study was evaluation of the significance of HLA-DRB1,-DRB3,-DRB4,-DRB5 associated alleles in the genetic susceptibility to sarcoidosis. We investigated 17 Polish 'families with' familial occurrence of the disease. Thirty three affected family members and 78 healthy relatives and 101 healthy individuals (control group) have been typed for HLA class II DR antigens. Assuming that relatives from families with two or more affected members are more susceptible to develop sarcoidosis we considered two classes: affected and healthy family members taken together (class 1, N = 111) and healthy control group (class 2, N = 101). HLA antigens from both classes were compared using a statistical pattern recognition method. This method, called k-NN method, assumes that objects (individuals) are described by a certain number of variables called features. Selected features that played an important role in the decision to which class an individual person would be classified were: HLA-DR7, HLA-DR2(16), HLA-DR1, HLA-DR5(12), HLA-DR6(14), HLA-DR6(13), HLA-DR9, HLA-DR5(11) and HLA-DRw52. K-NN method allowed to classify properly 76% of studied subjects to healthy or disease susceptible group. However, 24 out of 100 individuals would be misclassified which gives the total error rate of 0.24. We concluded that using HLA-DR antigens as features characterising every individual we can predict with high probability to which class ("high risk" or "healthy") individual would belong.

Case-Control Studies↗
PubMed1998

Contribution of HLA class II genes to susceptibility in achalasia.

Achalasia is a motor disorder of the esophagus resulting in functional obstruction. The cause of the lesion is unknown although genetic and immunologic factors have been suggested. An association with serological HLA epitopes has been previously reported. In this study, we have further examined this HLA class II association with susceptibility to achalasia by DNA based methods. Achalasia patients (n=40) and healthy controls (n=275), all Caucasians and unrelated, were included in the analysis. The strongest associations were with HLA-DQA1*0101 and two HLA-DQ alphabeta heterodimers having their alpha chain encoded by this allele. Moreover, relative risk was significantly higher in DQA1*0101 homozygotes as compared to heterozygotes and results suggested that DQB1*02 may have a protective role.

Alleles↗
PubMed2001

HLA class II antigens in South African Blacks with type I diabetes.

Type 1 diabetes mellitus is poorly characterised in many African communities, including South Africa, where little is known of the disease epidemiology. This study aimed to identify the HLA class II alleles associated with type 1 diabetes in a group of Zulu subjects in Durban, KwaZulu-Natal by PCR-SSP. The HLA alleles associated with type 1 diabetes included HLA-DQB*0302 (P<0.0001), DRB1*O9 (P<0.0001), DRB1*04 (P=0.002), DRB1*0301 (P=0.003), DQB*02 (P=0.004) and DQA*03 (P=0.035). Estimated haplotypes positively associated with type 1 diabetes included HLA-DRB1 *0301-DQA*0501, DRB1*04-DQA*03, DRB1*04-DQB*0302, DRB1*0301-DQB*0201, DQA*0501-DQB*0201 and DQA*03-DQB*0302. These findings are similar to those reported from Zimbabwe and other populations with type 1 diabetes.

Adult↗
PubMed1987

[Abnormal expression of HLA class II antigens in conjunctival epithelia in peripheral corneal ulcers].

Inflammatory mediators originating at the limbus seem to play an important role in the pathogenesis of peripheral corneal ulcers. In this paper, the immunohistological results of conjunctival biopsies of patients with corneal ulcers are reported. The most important result was that an abnormal HLA class II expression was found. The expression of HLA-DR was stronger than that of HLA-DQ and HLA-DP. A model of ulcer formation involving T-cells and lymphokines is presented.

Biopsy↗
PubMed1996

HLA class II associations in African-American female patients with Graves' disease.

Graves' disease (GD) is an autoimmune thyroid disease. Development of the disease phenotype is believed to be dependent on environmental factors and the action of several genes either in concert or in independent groups. Genes of, or closely associated to, the human leukocyte antigen (HLA) complex are important in determining genetic predisposition to GD in various ethnic groups. We previously reported that no significant HLA class I or -DR associations were detected in the total group of African-American patients with GD. To further investigate the associations of GD with HLA class II alleles, 52 unrelated African-American female patients with GD and 55 controls were typed for HLA-DRB1, -DQA1, and -DQB1, using sequence-specific oligonucleotide probes to analyze polymerase chain reaction amplified DNA. There were no significant differences in HLA distribution between patients and controls. These findings indicate that the contribution of HLA-DR and DQ regions to susceptibility to GD is small in African-American women.

Adult↗
PubMed2001

Type 1 diabetes environmental factors and correspondence analysis of HLA class II genes in the Yemenite Jewish community in Israel.

OBJECTIVE: The Israeli Yemenite Jewish community has displayed an exceptionally rapid increase in the frequency of type 1 diabetes, having the highest rate of all Israeli ethnic groups. We studied the role of the environment, in relation to the nature and frequency of HLA class II genes, to evaluate its possible involvement in the development of diabetes. RESEARCH DESIGN AND METHODS: We interviewed 196 elderly Yemenite women, who had immigrated to Israel as adults, in programmed encounters about signs and symptoms of type 1 diabetes, infant feeding customs, and infectious diseases in Yemen. We also performed HLA oligotyping of DRB1, DQA1, and DQB1 genes in 120 unrelated Yemenite Jews, including 44 type 1 diabetic patients and 76 healthy control subjects, and used these data in correspondence analysis comparing Yemenites with different Israeli ethnic groups. RESULTS: Interviews indicated that early exposure to cow's milk was very common in Yemen. However, none of the women could recall classical presentations of diabetes. HLA oligotyping showed that gene frequencies of non-Asp-57 (of the HLA-DQB chain) in the patients (0.94) and control subjects (0.6) were similar to those of other populations with a known high incidence of type 1 diabetes. Correspondence analysis revealed that Yemenite Jews are genetically distinct from other ethnic groups in Israel. CONCLUSIONS: The genetic distinctiveness of Yemenite Jews may explain their unusually high incidence of type 1 diabetes in Israel. Despite the presence of highly susceptible diabetogenic HL4 class II genes in this community, early exposure to cow's milk did not cause phenotypic expression of diabetes in Yemen. This finding suggests that in this population, either cow's milk does not play a crucial role in triggering diabetes, or environmentally conferred protection, such as frequent infectious disease in Yemen, was dominant.

Adult↗
PubMed2006

The presence of gestational diabetes is associated with increased detection of anti-HLA-class II antibodies in the maternal circulation.

PROBLEM: Gestational diabetes (GD) may be associated with temporarily reduced immune tolerance toward alloantigens for the time of pregnancy. The aim of this study was to assess anti-HLA-class I and -II antibodies as markers for an aberrant immunostimulation in women with GD. METHOD OF STUDY: The percentage of anti-HLA-class I and -II antibodies was estimated in women with GD, normal term delivery and fetal distress, which was confirmed by demonstrating low cord blood pH for this patient group. These antibodies may cross the placental barrier and cause interleukin-6 (IL-6) release from fetal monocytes by cross-linking monocytes with antibody-loaded cells. Therefore we estimated the percentage of IL-6-positive monocytes in the fetal circulation of these three patient groups. RESULTS: We found a significantly increased percentage of anti-HLA-class II in the circulation of women with GD. In comparison with women with normal term delivery, a significantly increased percentage of IL-6-positive monocytes was detected for women with GD and for women with fetal distress. Significantly decreased cord blood pH were detected for neonates born in the presence of fetal distress but not for neonates born in the presence of GD. CONCLUSIONS: Our results suggest that GD is associated with an increased humoral immune response against HLA-class II antigens.

Diabetes, Gestational↗