MHC class II alleles and haplotypes in patients with pemphigus vulgaris from India

Pemphigus vulgaris (PV) is a blistering disease of the skin and mucous membranes characterized by an autoantibody response against a keratinocyte adhesion molecule, desmoglein 3, causing acantholysis and blister formation. We compared high resolution MHC class II alleles and haplotype frequencies (HLA-DRB, DQA1 and DQB1) in 37 patients with PV to 89 haplotypes of normal relatives from New Delhi and Ahmedabad. We found that PV patients had significantly increased frequencies of DRB1*1404 (P < 0.0001), DQA1*0101 (P = 0.001), and DQB1*0503 (P < 0.0001). These associations were due to the increased frequencies of the haplotype HLA-DRB1*1404, DRB3*0202, DQA1*0101, DQB1*0503 in patients compared to control haplotypes (p < 0.0001). Also, patients from Ahmedabad had a significant increase in HLA-DQB1*0302 (p = 0.03). An identical amino acid sequence (Leu-Leu-Glu-Arg-Arg-Arg-Ala-Glu), in positions 67-74 of the beta domain of DRB alleles is restricted to some DR14 alleles. Therefore, there are three possible explanations for class II allele involvement in autoantibody in PV patients with class II haplotypes marked by HLA-DR14. First, the class II alleles could be markers for an unidentified susceptibility gene in linkage disequilibrium with them. Second, the primary association could be with DQB1*0503 and the association with HLA-DR14 alleles would be the result of linkage disequilibrium. Third, the HLA-DRB1 locus susceptibility could involve a specific amino acid sequence in the third hypervariable region shared by several HLA-DR14 alleles.     

Blocking of MHC class I antigens on leukemic B-cells enhances their conjugate formation with cytotoxic lymphocytes and their susceptibility to lysis

The role of major histocompatibility complex (MHC) class I antigens and adhesion molecules (AM) in the resistance of leukemic B-cells to cell-mediated cytotoxicity was investigated using cells from eight patients with B-chronic lymphocytic leukemia (B-CLL) and six patients with immunocytoma (IC). Both CLL and IC cells were completely resistant to natural killer (NK) and lymphokine activated killer (LAK) cytotoxicity and no binding to effector cells was observed, irrespectively of AM expression. Blocking of MHC class I antigens with monoclonal antibodies or their temporary elimination from leukemic B-cell surface by acid treatment resulted in a significant (p < 0.005) increase in both conjugate formation and susceptibility to lysis, thus suggesting the relevance of MHC class I expression on leukemic B-cells for the NK/LAK resistance phenomenon.     

Characterization of the peptide binding motif of a rhesus MHC class I molecule (Mamu-A*01) that binds an immunodominant CTL epitope from simian immunodeficiency virus

The majority of immunogenic CTL epitopes bind to MHC class I molecules with high affinity. However, peptides longer or shorter than the optimal epitope rarely bind with high affinity. Therefore, identification of optimal CTL epitopes from pathogens may ultimately be critical for inducing strong CTL responses and developing epitope-based vaccines. The SIV-infected rhesus macaque is an excellent animal model for HIV infection of humans. Although a number of CTL epitopes have been mapped in SIV-infected rhesus macaques, the optimal epitopes have not been well defined, and their anchor residues are unknown. We have now defined the optimal SIV gag CTL epitope restricted by the rhesus MHC class I molecule Mamu-A*01 and defined a general peptide binding motif for this molecule that is characterized by a dominant position 3 anchor (proline). We used peptide elution and sequencing, peptide binding assays, and bulk and clonal CTL assays to demonstrate that the optimal Mamu-A*01-restricted SIV gag CTL epitope was CTPYDINQM(181-189). Mamu-A*01 is unique in that it is found at a high frequency in rhesus macaques, and all SIV-infected Mamu-A*01-positive rhesus macaques studied to date develop an immunodominant gag-specific CTL response restricted by this molecule. Identification of the optimal SIV gag CTL epitope will be critical for a variety of studies designed to induce CD8+ CTL responses specific for SIV in the rhesus macaque.     

Evolution of a new nonclassical MHC class I locus in two Old World primate species

HLA-G is a nonclassical major histocompatibility complex (MHC) class I molecule that is expressed only in the human placenta, suggesting that it plays an important role at the fetal-maternal interface. In rhesus monkeys, which have similar placentation to humans, the HLA-G orthologue is a pseudogene. However, rhesus monkeys express a novel placental MHC class I molecule, Mamu-AG, which has HLA-G-like characteristics. Phylogenetic analysis of AG alleles in two Old World primate species, the baboon and the rhesus macaque, revealed limited diversity characteristic of a nonclassical MHC class I locus. Gene trees constructed using classical and nonclassical primate MHC class I alleles demonstrated that the AG locus was most closely related to the classical A locus. Interestingly, gene tree analyses suggested that the AG alleles were most closely related to a subset of A alleles which are the products of an ancestral interlocus recombination event between the A and B loci. Calculation of the rates of synonymous and nonsynonymous substitution at the AG locus revealed that positive selection was not acting on the codons encoding the peptide binding region. In exon 4, however, the rate of nonsynonymous substitution was significantly lower than the rate of synonymous substitution, suggesting that negative selection was acting on these codons.     

Shared epitope homozygosity' is strongly associated with rheumatoid arthritis in Turkey. Istanbul Rheumatology Study Group

OBJECTIVE: Associations with HLA-DRB alleles, implicated in the aetiopathogenesis of rheumatoid arthritis (RA), are found to be different in various ethnic groups. This study aimed to investigate DRB1 alleles in RA patients in Turkey. METHODS: The DRB region of the MHC was screened by polymerase chain reaction/sequence-specific oligonucleotide (PCR/SSO) hybridizations in 101 seropositive RA patients and compared with 101 healthy controls. RESULTS: Significant differences were in the frequencies of DRB1*0404 (12 vs 1, P = 0.003, OR = 13.5), *0401 (19 vs 4, P = 0.001, OR = 5.6) and *0408 (5 vs 0, P = 0.06, OR = 11.6) between RA patients and controls. The shared epitope (SE) was present in 70.2% of RA patients compared to 31.6% of controls (P < 0.0001, OR = 5.1). A double dose of SE was considerably more frequent in the RA group (21 vs 1, P < 0.0001, OR = 26.5). CONCLUSION: These results support the reported positive association of RA with SE in seropositive patients in Turkey, and emphasize 'SE homozygosity' as the most strongly associated genetic susceptibility marker for RA.     

Activation of DNA synthesis and expression of the JE gene by catalase in mouse osteoblastic cells: possible involvement of hydrogen peroxide in negative growth regulation

Type I diabetes susceptibility genes have been identified within the major histocompatibility complex (MHC) on chromosome 6p21.3 and near the VNTR/insulin region on chromosome 11p15.5. We have used polymorphic dinucleotide repeat markers to search the human genome for additional susceptibility genes in 162 type I diabetic families with an affected sibling pair. We report that an additional susceptibility gene is located on chromosome 2q31 near HOXD8 (P < 10(-5), maximum logarithm of odds score = 4.8) in an analysis of affected sibling pairs having specific human leukocyte antigen (HLA) and hypervariable nucleotide tandem repeat (VNTR)/insulin gene haplotypes (absence of high-risk HLA-DR3/4 haplotypes and presence of homozygous high-risk class I VNTR alleles). These results suggest the interaction of a minimum of three genes in the pathogenesis of type I diabetes in humans.     

Serological responses of patients with ectopic pregnancy to epitopes of the Chlamydia trachomatis 60 kDa heat shock protein

Clinical and histopathological correlations of immunoreactivity to Chlamydia trachomatis and to epitopes of the C. trachomatis 60 kDa heat shock protein (hsp60) among women with ectopic pregnancy were evaluated in a case-control study. Serological responses to 13 synthetic peptides corresponding to major epitopes of the chlamydial hsp60 were determined in 67 women treated for ectopic pregnancy and 45 women with uncomplicated pregnancy in utero. Plasma cell salpingitis was detected in 29 (43.3%) of the ectopic patients. Its presence correlated with antibodies to two hsp60 epitopes, encompassing amino acids 260-271 and 411-422 (P = 0.02). Antibodies to these two epitopes, along with five other epitopes, also correlated with peritubal adhesion formation in ectopic pregnant patients (P < 0.01). Antibodies to epitopes 260-271 and 188-199 also correlated with a history of pelvic inflammatory disease (PID; P = 0.05). Patients with ectopic pregnancy were also more likely than their intrauterine pregnant controls to have present anti-chlamydial immunoglobulin G (P < 0.005). Women positive for both C. trachomatis and hsp60 epitope antibodies had an increased prevalence over controls of salpingitis, pelvic adhesions or history of PID (P < 0.05). In contrast, patients who were positive for only C. trachomatis antibodies or only hsp60 epitope antibodies did not differ from antibody-negative patients in each of these categories.     

Effectiveness of postinoculation (R)-9-(2-phosphonylmethoxypropyl) adenine treatment for prevention of persistent simian immunodeficiency virus SIVmne infection depends critically on timing of initiation and duration of treatment

(R)-9-(2-Phosphonylmethoxypropyl)adenine (PMPA), an acyclic nucleoside phosphonate analog, is one of a new class of potent antiretroviral agents. Previously, we showed that PMPA treatment for 28 days prevented establishment of persistent simian immunodeficiency virus (SIV) infection in macaques even when therapy was initiated 24 h after intravenous virus inoculation. In the present study, we tested regimens involving different intervals between intravenous inoculation with SIV and initiation of PMPA treatment, as well as different durations of treatment, for the ability to prevent establishment of persistent infection. Twenty-four cynomolgus macaques (Macaca fascicularis) were studied for 46 weeks after inoculation with SIV. All mock-treated control macaques showed evidence of productive infection within 2 weeks postinoculation (p.i.). All macaques that were treated with PMPA for 28 days beginning 24 h p.i. showed no evidence of viral replication following discontinuation of PMPA treatment. However, extending the time to initiation of treatment from 24 to 48 or 72 h p.i. or decreasing the duration of treatment reduced effectiveness in preventing establishment of persistent infection. Only half of the macaques treated for 10 days, and none of those treated for 3 days, were completely protected when treatment was initiated at 24 h. Despite the reduced efficacy of delayed and shortened treatment, all PMPA-treated macaques that were not protected showed delays in the onset of cell-associated and plasma viremia and antibody responses compared with mock controls. These results clearly show that both the time between virus exposure and initiation of PMPA treatment as well as the duration of treatment are crucial factors for prevention of acute SIV infection in the macaque model.     

Fusion of the craniocervical transition with "CerviFix" after survived atlanto-occipital dislocation

The mechanism by which particular MHC class II alleles mediate susceptibility to a given autoimmune disease is unknown. During the past year, reports have indicated that the effects of MHC class II alleles which protect against type I diabetes in the nonobese diabetic mouse strain may, in some cases, be due to negative selection of diabetogenic T cell receptors and, in other cases, to positive selection of other T cells with a suppressive action on the diabetic process. Progress towards understanding the mechanisms of susceptibility continues to lag.     

Use of statistical programs for nonparametric tests of small samples often leads to incorrect P values: examples fromAnimal Behaviour

To determine if serum antibody response to the 60-kDa chlamydial heat-shock protein (Chsp60) was associated with scarring trachoma, responses to Chlamydia trachomatis and to Chsp60 from 148 Gambian subjects with trachomatous scarring and from 148 controls without clinical evidence of disease from trachoma-endemic communities were characterized. Chsp60 response was found in 32% of cases and 16% of controls (P < .001). Although C. trachomatis titer was also higher in cases than controls, the prevalence of Chsp60 response between the 2 groups remained significantly different after stratifying for C. trachomatis titer (weighted odds ratio [OR] = 2.1, P = .02). Chsp60 response and C. trachomatis serovar A titer of > or =128 were independently associated with scarring trachoma. The presence of HLA class II allele DRB1*0701 was positively correlated with Chsp60 response (OR = 2.6, P = .02), and DQB1*0301 and DQB1*0501 were negatively associated (OR = 0.42, P < .001; OR = 0.55, P = .46, respectively).     

Hypoxaemia and supplemental oxygen therapy in the first 24 hours after myocardial infarction: the role of pulse oximetry

SIV infection of rhesus macaques is an excellent model for HIV infection of humans. Unfortunately, it is has been difficult to identify macaques expressing particular MHC class I alleles. Here we describe the use of PCR-SSP for Mamu-A*01 typing of rhesus macaques. The Mamu-A*01 allele was amplified from genomic DNA using Mamu-A*01-specific primers and positive PCR products were directly sequenced. Our technique identified 15 Mamu-A*01-positive animals of 68 tested. We validated our molecular analysis by showing that lymphocytes from 8 Mamu-A*01-positive animals expressed Mamu-A*01 as determined by immunoprecipitation and 1-D IEF. The technical simplicity and accuracy of this typing method should facilitate selection of Mamu-A*01-positive rhesus macaques for AIDS virus pathogenesis and vaccine studies.     

Scarring trachoma is associated with polymorphism in the tumor necrosis factor alpha (TNF-alpha) gene promoter and with elevated TNF-alpha levels in tear fluid

Tumor necrosis factor alpha (TNF-alpha) may play a central role in the disease pathogenesis which occurs as a consequence of chlamydial infection. To investigate the importance of TNF-alpha gene promoter polymorphisms and TNF-alpha levels in tear fluid in scarring trachoma, a large matched-pair case-control study was performed in The Gambia. The -308A allele was present in a higher proportion of patients (28.4%) than controls (18.4%), with an increasing association for homozygotes (chi2 for trend, P = 0.032; allele frequency, 0.163 in patients and 0.099 in controls; chi2, P = 0.025). For the -238A allele, the association was similar but not significant. The disease association was highly significant when the number of either -308A or -238A sites in an individual was considered (P = 0.003). TNF-alpha promoter alleles are tightly linked to some HLA class I and II alleles, but multivariate analysis confirmed that the disease associations were independent of HLA, although a class I allele, A*6802, is also associated with disease. TNF-alpha was more frequently detected in tear samples from patients (27.6%) than from controls (15.9%), increasingly so for higher levels of detectable TNF-alpha (P = 0.015). Among patients, detectable TNF-alpha in tears was highly associated with the presence of ocular chlamydial infection (P < 0.001). The results indicate that TNF-alpha plays a major role in the tissue damage and scarring which occurs as a consequence of Chlamydia trachomatis infection.     

The effect of training and duration of surgery on adhesion formation in the rabbit model

In order to evaluate the effect of training upon postoperative adhesions, standard bipolar and mechanical, nonopposing injuries were performed in the uterine horns and side walls of 52 mature female rabbits using a conventional three-puncture laparoscopy, by an endoscopic surgeon with limited experience. An additional injury, either bipolar or mechanical or both, was performed in the retro-uterine space. With experience, the duration of surgery decreased progressively from 12 +/- 2 to 8 +/- 1 min in the first and last 10 animals respectively. The amount of perioperative bleeding was not affected by experience. With experience the postoperative adhesions decreased in extent (P = 0.0001), tenacity (P = 0.004), type (P = 0.002) and inflammation (P = 0.003) and for total score (P = 0.0002). These changes were correlated with the briefer duration of surgery but not with the amount of perioperative bleeding. The strong correlations of adhesion scores in the pouch of Douglas, and around both uterine horns confirmed the importance of the inter-animal variability in making adhesions. By logistic regression, the adhesions in the pouch of Douglas were explained simultaneously by the adhesions on the uterine horns (P = 0.0004, thus correcting for inter-animal variability) by the amount of bleeding (P = 0.01) and the duration of surgery (P = 0.05). No major differences were found in adhesions following a mechanical or a bipolar injury or following such a lesion in the pouch of Douglas or at the uterine horns. In conclusion, experience, expressed by the duration of surgery and to a lesser extent perioperative bleeding, is a major co-factor in postoperative adhesions, suggesting that duration of surgery should be strictly standardized in endoscopic adhesion studies. The important inter-animal variability can be circumvented by using a standard control lesion, making each animal its own control.     

DRB1*15 and DRB1*03 extended haplotype interaction in primary Sj?gren's syndrome genetic susceptibility

OBJECTIVE: Sj?gren's syndrome (SS) is a chronic autoimmune disease with a genetic component. Among the genetic factors, the role of HLA class II genes has been suggested and a positive association with DRB1*03 allele has been described. However, there is no consensus on a unique HLA locus for this disease nor on the role of the HLA gene product in the disease. The aim of this study was to analyse prospectively MHC region involvement in the genetic susceptibility to SS by studying DRB1, DQB1, DPB1, TAP1, TAP2 genes and TNF microsatellites in a population of 45 primary SS patients. METHODS: All the polymorphisms studied were analysed at the genomic level using PCR-based methodologies. RESULTS: Concerning HLA class II alleles, the highest relative risk to develop the disease was associated with the DRB1*15-DRB1*0301 heterozygous genotype (17.8% vs 3.5% in controls - pc < 0.005, OR = 5.96). Analysing other genes located on the same region allowed us to further determine the DRB1 haplotypes at risk. For instance, the DRB1*0301 haplotype involved in the genetic susceptibility to SS was more often associated with the DPB1* 0201 and TNF-a2 alleles in SS patients than in controls. Moreover, all the DRB1*15-DRB1*0301 SS patients were TAP1-0101, TAP2-0101 homozygous, allowing us to deduce the extended genotype at risk as DRB1*15, TAP1-0101, TAP2-0101/DRB1*0301, TAP1-0101, TAP2-0101 which was carried by only 3 controls out of the 130 tested (p < 0.01, OR = 6.68). CONCLUSION: This study confirmed the role of the MHC region in the susceptibility to Sj?gren's disease, and for the first time suggests a synergistic interaction between two HLA-DRB1 extended haplotypes in the genetic mechanisms controlling the disease.     

Oral budesonide for prevention of postsurgical recurrence in Crohn's disease. The IOIBD Budesonide Study Group

Results of genetic association studies in UC are conflicting. We propose that the power of candidate gene studies will increase when disease heterogeneity is taken into account. Phenotype frequencies of molecularly defined HLA-DR alleles, polymorphisms in the tumour necrosis factor-alpha (TNF-alpha), lymphotoxin-alpha (LT-alpha), IL-1 receptor antagonist (IL-1Ra) and IL-1beta genes were determined in 98 clinically well characterized UC patients with a mean period of follow up of 10 years, and ethnically matched healthy controls (HC). The alleles HLA-DRB1*0103 (phenotype frequency 6% versus 0.2%; P = 0.0002; odds ratio (OR) 27.6) and DRB1*15 (41% versus 26%; P = 0. 001; OR = 2.0, compared with HC) were associated with overall disease susceptibility. Subgroup analysis revealed that DRB1*15 was only increased in females (53% versus 24%; P < 0.0001; OR = 3.5), but not in males. With regard to disease localization, all DRB1*0103+ patients had extensive disease (P < 0.002; OR = 33.5), and DRB1*15 was found in 59% of females with extensive colitis (P < 0.0001; OR = 4.4). DRB1*0103 was significantly increased in patients undergoing colectomy (P < 0.0002; OR = 84). No association between overall disease susceptibility and the cytokine gene polymorphisms were found. Subgroup analysis revealed several significant associations, but most did not retain significance when corrected for multiple comparisons. However, a noticeable finding was that haplotype TNF-C was significantly associated with progression in extent of disease (P = 0.003, OR = 20.4). This study provides additional evidence for the role of DRB1 alleles in the susceptibility to UC, and supports the hypothesis that these alleles may determine the severity of the disease. The cytokine gene polymorphisms evaluated in this study do not seem to be strong risk factors for the overall disease susceptibility in UC, but may be involved in determining the severity of the disease.     

Role of major histocompatibility complex class I antigens in modulating the performance of murine tumour cells in cold target competition assays

The role of class I major histocompatibility complex (MHC) antigen levels on the ability of five murine tumour cell lines (YAC, P815, EL4, SP20 and L929) to competitively inhibit their own lysis, as well as the lysis of other targets by lymphokine-activated killer (LAK) effector cells was examined. Basal LAK susceptibilities of the cell lines were in the order P815 > YAC > SP20 > EL4 > L929, whereas the basal class I MHC antigen levels were in the order P815 > SP20 > L929 > YAC > EL4. Treatment with interferon-gamma (IFN-gamma) induced augmentation of class I MHC antigen levels on all cell lines. A concomitant decline in LAK susceptibility was seen for P815, YAC, SP20 and L929 cells, but not for EL4 target cells. On the basis of competition results, tumour cells appear to fall into two groups (group 1: P815, YAC and SP20; group 2: EL4 and L929). Members of each group could in general competitively inhibit the lysis of cell lines of their own group only. Treatment with IFN-gamma suppressed the ability of all tumour cell lines, except EL4, to cause competitive inhibition. These results support the proposition that class I MHC antigens may interfere with the recognition of target cells by effector LAK cells.     

Immunodominance of a single CTL epitope in a primate species with limited MHC class I polymorphism

MHC class I molecules play a crucial role in immunity to viral infections by presenting viral peptides to cytotoxic T lymphocytes. One of the hallmarks of MHC class I genes in outbred populations is their extraordinary polymorphism, yet the significance of this diversity is poorly understood. Certain species with reduced MHC class I diversity, such as the cotton-top tamarin (Saguinus oedipus), are more susceptible to fatal viral infections. To explore the relationship between this primate's limited MHC class I diversity and its susceptibility to viruses, we infected five cotton-top tamarins with influenza virus. Every tamarin recognized the same immunodominant CTL epitope of the influenza nucleoprotein. Surprisingly, this nucleoprotein peptide was bound by Saoe-G*08, an MHC class I molecule expressed by every cotton-top tamarin. Two tamarins also made a subdominant response to an epitope of the matrix (M1) protein. This peptide appeared to be bound by another common MHC class I molecule. With the exception of an additional subdominant response to the polymerase (PB2) protein in one individual, no other influenza-specific CTL responses were detected. In populations or species with limited MHC class I polymorphism like the cotton-top tamarin, a dependence on shared MHC class I molecules may enhance susceptibility to viral infection, since viruses that evade MHC class I-restricted recognition in one individual will likely evade recognition in the majority of individuals.     

The protein tyrosine kinase p56lck regulates cell adhesion mediated by CD4 and major histocompatibility complex class II proteins

The CD4 protein is expressed on a subset of human T lymphocytes that recognize antigen in the context of major histocompatibility complex (MHC) class II molecules. Using Chinese hamster ovary (CHO) cells expressing human CD4, we have previously demonstrated that the CD4 protein can mediate cell adhesion by direct interaction with MHC class II molecules. In T lymphocytes, CD4 can also function as a signaling molecule, presumably through its intracellular association with p56lck, a member of the src family of protein tyrosine kinases. In the present report, we show that p56lck can affect cell adhesion mediated by CD4 and MHC class II molecules. The expression of wild-type p56lck in CHO-CD4 cells augments the binding of MHC class II+ B cells, whereas the expression of a mutant p56lck protein with elevated tyrosine kinase activity results in decreased binding of MHC class II+ B cells. Using site-specific mutants of p56lck, we demonstrate that the both the enzymatic activity of p56lck and its association with CD4 are required for this effect on CD4/MHC class II adhesion. Further, the binding of MHC class II+ B cells induces CD4 at the cell surface to become organized into structures resembling adhesions-type junctions. Both wild-type and mutant forms of p56lck influence CD4-mediated adhesion by regulating the formation of these structures. The wild-type lck protein enhances CD4/MHC class II adhesion by augmenting the formation of CD4-associated adherens junctions whereas the elevated tyrosine kinase activity of the mutant p56lck decreases CD4-mediated cell adhesion by preventing the formation of these structures.     

Antibodies to chlamydia trachomatis in semen and relationship with parameters of male fertility

To screen for infection with Chlamydia trachomatis in semen samples from asymptomatic men in couples consulting for infertility and to determine the relationship of seminal chlamydial antibodies with clinically relevant parameters of male fertility, 197 randomly chosen patients were enrolled in a prospective study. The median duration of infertility was 4 years (range 1-18). Screening for C. trachomatis and chlamydial antibodies of the immunoglobulin (Ig) A and IgG classes were performed in ejaculates and, in parallel, endocervical material from the partners of the patients and serum samples from both partners were evaluated. A comprehensive examination of semen quality included sperm analyses, semen cultures, local antisperm antibody (ASA) testing, the determination of potential infection markers, and sperm-cervical mucus interaction testing in vitro (SCMPT) and in vivo (post-coital testing). Chlamydial IgA antibodies were found in the semen samples of 18.8% (37/197) of the patients, while chlamydial IgG antibodies were found in 8.1% (16/197) of the patients. Screening for C. trachomatis was negative in all semen and cervical specimens. Only 5.5% of men remembered a past genital infection. Chlamydia antibodies (IgA/Ig/G) in semen were significantly correlated with chlamydia IgG antibodies in serum samples (P < 0.001). No marked relationship was found between the presence of seminal chlamydial antibodies and the major parameters of sperm analysis, semen cultures, local ASA and sperm penetration testing as an indicator of functional capacity. Seminal chlamydial antibodies were not significantly associated with potential infection or inflammation markers in aliquots of the same ejaculates. However, a significant relationship of chlamydial antibodies in patients' semen with past genital infections of their female partners was found with clinical relevance for a tubal infertility factor. The results indicate that in asymptomatic patients the presence of chlamydial antibody IgA or IgG in semen is not associated with reduced semen quality, potential seminal infection markers or impaired functional capacity as important determinants of male fertility; however, seminal chlamydial antibodies suggesting a previous sexually transmitted disease are significantly related to a tubal infertility factor of female partners.     

Helicobacter pylori infection in immunized mice lacking major histocompatibility complex class I and class II functions

The role of major histocompatibility complex (MHC) class I- and class II-restricted functions in Helicobacter pylori infection and immunity upon oral immunization was examined in vivo. Experimental challenge with H. pylori SS1 resulted in significantly greater (P 相似文献