Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Highly purified, detergent-solubilized HLA-A and -B antigens and HLA-D antigens were separately incorporated into liposomes. Detergent-solubilized transplantation antigens, but not papain-solubilized antigens lacking the membrane-integrated portions of the molecules, were bound to the liposomes. A considerable portion of the liposome-bound antigens displayed accessible antigenic sites, suggesting that they were oriented in the right-side-out direction. Liposomes containing the HLA-A and -B antigens or the HLA-D antigen interacted similarly with bacteria. The two types of liposomes bound efficiently to two strains of Neisseria catarrhalis (now classified as Branhamella catarrhalis) and to one strain of Haemophilus influenzae, weakly to one strain of Escherichia coli, and not at all to another strain of E. coli. The binding between the HLA antigen-containing liposomes and one strain of N. catarrhalis was abolished when Fab fragments directed against the heavy chains of HLA-A and -B antigens or against HLA-D antigens, respectively, were added. In contrast Fab fragments against beta(2)-microglobulin did not measurably impede the bacteria-liposome interaction, suggesting that, with regard to the HLA-A and -B antigens, the heavy, but not the light, chains interacted with the bacteria. Additional experiments showed that N. catarrhalis preferentially interacted with transplantation antigens when mixed with detergent-solubilized lymphocyte membrane glycoproteins. These data suggest that HLA-A and -B and HLA-D antigens may have the function of interacting with foreign antigens such as bacteria.
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PMID:Binding of HLA antigen-containing liposomes to bacteria. 28 37

Meningitis is the most important cause of acquired postnatal deafness and neurologic disorders in children. To determine if cell-mediated immunity is casually related to the pathogenesis of bacterial meningitis, T cell subsets were quantitated from blood of the 29 children with clinical and bacteriologic diagnosis of Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis bacterial meningitis. The CD4+ T cells increased and CD8+ T cells decreased in patients with meningitis as compared to patient control subjects (bacterial infections without meningitis) and normal healthy control subjects. An elevated percentage of CD25+ (interleukin-2 receptors) and HLA-DR+ (immune-response gene-associated antigen) T cells were detected from all patients with meningitis. All 29 patients with meningitis had highly elevated CD4+ CD45R+ (suppressor-inducer) cells and reciprocally depressed CD4+ CDw29+ (helper-inducer) cells compared with healthy age-matched normal and patient control subjects. These findings indicate characteristic immunologic T cell abnormalities from meningitis. The abnormal increase in the CD4+ CD45R+ suppressor-inducer or "virgin" cells and expression of activation antigens on T cells may be of help in future understanding of abnormal immune reactions from bacterial meningitis. However, deficiency of the CD4+ CDw29+ helper-inducer or "memory" cells may contribute to the impaired helper function for B cell-induced protective antibody synthesis to bacterial capsular polysaccharides found in this disease.
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PMID:Bacterial meningitis: T cell activation and immunoregulatory CD4+ T cell subset alteration. 171 Jun 32

Primary B-cell immunodeficiency is relatively frequent and may result in recurrent bacterial infections involving notably the respiratory tract, and in chronic severe enteroviral infections in patients with agammaglobulinaemia. Selective IgG2 isotype deficiency results in pneumococcal, Haemophilus influenzae and pseudomonal infections, since it is associated with defective production of antibodies that are specifically directed against bacterial capsular polysaccharides. Progress has recently been achieved in the determination of genetic and molecular bases of some of these immunodeficiencies. In X-linked agammaglobulinaemia, the abnormal gene has been located on the long arm of the X chromosome (Xq22-23); the intrinsic B-cell abnormality blocks differentiation at the pre-B stage, before the genes coding for light chain immunoglobulins are rearranged. There is now a strong suspicion that IgA deficiency, hypoglobulinaemia with variable expression and some selective IgG isotype deficiencies are three ways of expressing one single abnormality a genetic factor of which is located in the class III region of the HLA complex and perhaps also associated with HLA class II DQ. Treatment of deficient IgG production with intravenous immunoglobulin has thoroughly altered the prognosis of these diseases. Complete IgA deficiency carries a risk of accident by production of anti-IgA antibodies, which means that patients with isolated IgA deficiency should not be treated, that these antibodies should systematically be looked for in patients with IgA deficiency associated with partial deficiency of other immunoglobulins, and that these patients should be treated with IgA-free immunoglobulin preparations.
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PMID:[Primary immune deficiencies of B-lymphocytes]. 204 14

Ig class- and IgA subclass-specific immune responses to protein and polysaccharide Ag were studied in serum, external secretions, and at the single cell level in peripheral blood of systemically immunized adults. Immunization with tetanus toxoid induced predominantly IgG antibody responses in serum and in the PBMC. The IgA antibody response was low, and was mostly of the IgA1 subclass. In contrast, immunization with polysaccharide Ag (Haemophilus influenzae type b, Neisseria meningitidis serogroup A, C, Y, W-135, and Streptococcus pneumoniae capsular polysaccharides) elicited a major IgA response predominantly of the IgA2 isotype. Analysis of the molecular forms of secreted IgA antibodies indicated that polymers were produced early after immunization, irrespective of the nature of the Ag. When compared with serum antibody and to PBMC cell responses, systemic immunization with polysaccharides induced a minor salivary response dominated by IgG and IgM antibodies. In contrast, the presence of antipolysaccharide antibodies in bile, irrespective of their isotype, paralleled the serum response 14 days after the immunization with polysaccharide Ag. These results suggest that biliary Ig were mostly derived from serum. Different patterns of the expression of MHC class II Ag on T cells, B cells, and monocytes during the course of immunization with protein or polysaccharide Ag were observed: whereas protein Ag induced a high frequency of HLA-DP- and HLA-DR-expressing cells early in the course of immunization, polysaccharide vaccines elicited low and protracted increases of HLA-DP+ T cells. Polysaccharide vaccine covalently coupled to a protein carrier induced a higher frequency of antipolysaccharide antibody-secreting cells in peripheral blood and increased the IgG to IgA ratio among polysaccharide-specific antibody-secreting cells.
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PMID:Immunization of humans with polysaccharide vaccines induces systemic, predominantly polymeric IgA2-subclass antibody responses. 211 Feb 13

Three recent cases of inherited deficiency of the seventh component of complement (C7) associated with recurrent infectious meningitis are described. Two cases were associated with meningococcal meningitis, the third is the first case report of C7 inherited deficiency associated with Haemophilus parainfluenzae meningitis. Family studies are consistent with inheritance and non-HLA-linked, autosomal codominant trait of the C7 deficiency. The three patients have remained well, following antibiotic treatment.
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PMID:[Familial deficiency of complement factor 7: association with bacterial meningitis. Apropos of 3 recent cases]. 304 43

Because Alaskan Eskimos have the greatest known endemic risk of Haemophilus influenzae type b (Hib) disease and represent a comparatively homogeneous population, we selected this population to evaluate the presence or absence of an association of 35 genetic markers (alleles or allotypes) at 12 chromosomal loci with susceptibility to both invasive Hib disease risk and level of Hib anticapsular antibody. We studied nearly all Alaskan Eskimo children who had had invasive Hib disease between 1971 and 1982 in southwestern Alaska (n = 103) and an equivalent number of controls matched for age, race, and village of residence, and verified not to have had proved or suspected Hib disease. We found no significant associations with Hib disease for the single alleles of HLA-A, -B, -C, -DR, Gm, Km, Am, Kidd, MNSs, ABO, esterase D, or glutamate pyruvate transaminase loci. However, we observed a significant interaction of two loci, Gm(a;..;g,s,t) allotype and HLA-DR8 (P = 0.002), with increased Hib disease susceptibility, and an interaction of the same Gm allotype and HLA-DR5 with decreased disease susceptibility (P = 0.01). We also compared the level of anticapsular antibody to Hib with each genetic marker and two-locus interactions, but no genetic association with antibody level was found. We conclude that some genetic factors contribute to the susceptibility to invasive Hib disease in this population.
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PMID:Genetic factors in Haemophilus influenzae type b disease susceptibility and antibody acquisition. 349 97

We have studied 50 Caucasoid children under 7 years of age with Haemophilus influenzae b disease. Half of the patients (Group A) had invasive disease shown by positive blood and/or spinal fluid culture. The other half (Group B) had noninvasive disease characterized by fever, nasopharyngitis, negative blood culture, and positive throat culture. Age, number of other siblings under 12 years old in the family, immune response, antibody production and genetic markers were compared in the two groups. Significant difference between the two groups was only seen in their genetic markers. HLA-B12 was present in 52% of Group A patients as opposed to 16% in Group B patients (P less than .01). HLA-Bw40 was present in 24% of group B patients and absent in all Group A patients (P less than .01). These findings would suggest that susceptibility and resistance towards developing invasive type b disease may be genetically determined.
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PMID:Occurrence of HLA types in H. influenzae type B disease. 616 96

Genes associated with immunoglobulin (Ig) allotype determinants are important in regulation of immune responses to bacterial polysaccharides. Furthermore, loci associated with Ig allotypes have been reported to interact with those associated with the major histocompatibility complex and affect susceptibility to certain diseases. In the present study we determined the frequencies of certain Gm phenotypes in patients with Haemophilus meningitis or epiglottitis and in controls. HLA-A, -B and -DR specificities had previously been determined in the majority of these subjects. Although no Ig phenotype was associated with increased or decreased relative risk of disease, the frequencies of several combinations of HLA specificities and Ig phenotypes were significantly different from those of controls. Thus, for subjects with the Gm phenotype (1, 3, 17; 23; 5, 13, 21), the risk of Haemophilus meningitis or epiglottitis was lower in individuals with HLA-B5 than in those without this specificity (odds ratio less than 0.1, P less than 0.004). In contrast, for subjects with the closely related Gm phenotype differing only by the absence of Gm(23), (1, 3, 17; ; 5, 13, 21), the risk of disease was higher in those with HLA-DR3 than in individuals who lacked DR3 (odds ratio = 11.0, P = 0.02). Although the present data require confirmation in an independent sample, they suggest that complex interactions between genes at two independent loci controlling HLA and Ig allotypes, respectively, may affect susceptibility to Haemophilus disease.
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PMID:Interactive effect of genes associated with immunoglobulin allotypes and HLA specificities on susceptibility to Haemophilus influenzae disease. 652 Apr 6

Immunity to poliovirus, diphtheria and Haemophilus influenzae type b (Hib) was studied in 16 adult recipients of a bone marrow transplant from an HLA-identical sibling donor in order to evaluate the need for revaccinations. T-cell depletion was not done in any case. The donors and patients were studied before bone marrow transplantation (BMT) and the patients 1, 3, 6, and 12 months later. Prior to the BMT 10 of 11 patients were immune (titre > or = 4) to all vaccine poliovirus types by a standard microneutralization assay. At 12 months after BMT only two of seven patients were immune to all vaccine types, and none had immunity against an antigenically altered poliovirus type 3 strain Finland. The geometric means of antibody titres against poliovirus types 1, 2, and 3 strain Saukett and strain Finland declined gradually after 1 month postgrafting, being 4.4, 5.4, 3.3, and 1.3 respectively at 12 months after BMT. At 1 year 6 of 11 patients had immunity against diphtheria by a toxin neutralization method, but the antitoxin geometric mean level had decreased to a barely protective level, 0.01 IU/ml. The geometric mean Hib antibody concentration decreased during the first 6 months after BMT and thereafter increased slightly. A significant proportion of BMT recipients lose their protection against polio, diphtheria and Hib, and revaccinations are necessary.
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PMID:Loss of protective immunity to polio, diphtheria and Haemophilus influenzae type b after allogeneic bone marrow transplantation. 870 45

The tyrosine phosphatase IA-2 is a molecular target of pancreatic islet autoimmunity in type 1 diabetes. T-cell epitope peptides in autoantigens have potential diagnostic and therapeutic applications, and they may hold clues to environmental agents with similar sequences that could trigger or exacerbate autoimmune disease. We identified 13 epitope peptides in IA-2 by measuring peripheral blood T-cell proliferation to 68 overlapping, synthetic peptides encompassing the intracytoplasmic domain of IA-2 in six at-risk type 1 diabetes relatives selected for HLA susceptibility haplotypes. The dominant epitope, VIVMLTPLVEDGVKQC (aa 805-820), which elicited the highest T-cell responses in all at-risk relatives, has 56% identity and 100% similarity over 9 amino acids (aa) with a sequence in VP7, a major immunogenic protein of human rotavirus. Both peptides bind to HLA-DR4(*0401) and are deduced to present identical aa to the T-cell receptor. The contiguous sequence of VP7 has 75% identity and 92% similarity over 12 aa with a known T-cell epitope in glutamic acid decarboxylase (GAD), another autoantigen in type 1 diabetes. This dominant IA-2 epitope peptide also has 75-45% identity and 88-64% similarity over 8-14 aa to sequences in Dengue, cytomegalovirus, measles, hepatitis C, and canine distemper viruses, and the bacterium Haemophilus influenzae. Three other IA-2 epitope peptides are 71-100% similar over 7-12 aa to herpes, rhino-, hanta- and flaviviruses. Two others are 80-82% similar over 10-11 aa to sequences in milk, wheat, and bean proteins. Further studies should now be carried out to directly test the hypothesis that T-cell activation by rotavirus and possibly other viruses, and dietary proteins, could trigger or exacerbate beta-cell autoimmunity through molecular mimicry with IA-2 and (for rotavirus) GAD.
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PMID:T-cell epitopes in type 1 diabetes autoantigen tyrosine phosphatase IA-2: potential for mimicry with rotavirus and other environmental agents. 960 76


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