Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Humoral immunity to bacterial antigens was investigated in 68 tissue typed and glucose tolerance tested first degree blood relatives of insulin dependent diabetics (IDD). The data were compared with those obtained in 60 IDDs and in 55 healthy controls. The prevalence of bacterial antibodies to E. coli, staphylococci, pertussis and diphtheria toxins were just slightly, but not significantly reduced in the blood relations compared with controls. Incidence of antibacterial antibodies was almost identical in blood relations with impaired and in those with normal glucose tolerance. By contrast, antibody formation to E. coli and staphylococci (p less than 0,0005, p less than 0,0005) respectively was significantly impaired in IDD. No correlation between genes of the major histocompatibility complex and humoral antibacterial immunity could be observed in IDD and blood relations. In conclusion, antibacterial antibody formation was found to be severely impaired in IDD patients but to be almost normal in blood relations of insulin dependent diabetics. These findings suggest that the humoral antibacterial immunodeficiency observed in IDD is a disease associated process probably independent of major histocompatibility complex linked genes.
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PMID:Humoral antibacterial immunity in first degree relatives of insulin-dependent diabetics. 71 Jun 77

The interaction of the immunodominant pertussis toxin peptide containing residues 30-42 (p30-42) with soluble DR1 molecules and the T-cell receptor (TCR) of 12 DR1-restricted human T-cell clones has been analyzed. Peptide analogues of p30-42 containing single alanine substitutions were used in DR1-binding and T-cell proliferation assays to identify the major histocompatibility complex and TCR contact residues. Each T-cell clone was found to recognize p30-42 with a different fine specificity. However, a common core comprising amino acids 33-39 was found to be important for stimulation of all T-cell clones. Within this core two residues, Leu33 and Leu36, interact with the DR1 molecule, whereas Asp34, His35, Thr37, and Arg39 are important for TCR recognition in most of the clones. Computer modeling of the structure of p30-42 showed that an alpha-helical conformation is compatible with the experimental data. The analysis of TCR rearrangement revealed that the peptide was recognized by T-cell clones expressing different variable region alpha (V alpha) and variable region beta (V beta) chains, although a preferential use of V alpha 8-V beta 13 and V alpha 11-V beta 18 combinations was found in clones from the same donor. Understanding the details of the interaction of antigenic peptides with the major histocompatibility complex and TCR molecules should provide the theoretical basis to design T-cell epitopes and obtain more immunogenic vaccines.
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PMID:Interaction of the pertussis toxin peptide containing residues 30-42 with DR1 and the T-cell receptors of 12 human T-cell clones. 131 75

Rats were injected intraperitoneally from birth on with a mouse monoclonal antibody (R73) to a constant determinant of the rat T cell receptor (TcR)2. Throughout the observation period (6 months), TcR2+ cells in peripheral lymphoid organs and blood were absent in treated animals with the exception of few (less than 10%) cells with a tenfold reduced TcR2 density; peripheral TcR2-CD3+ cells, i.e. most likely TcR1+ T cells, were increased in frequency. Among thymocyte subpopulations, only those expressing the TcR2 at a high level were reduced in number. The lack of a visible effect on immature thymocytes may, however, be due to the fact that despite high serum levels, thymic R73 determinants were incompletely saturated. Spleen and lymph node cells from TcR2-suppressed rats were completely unresponsive in mixed lymphocyte reaction (two fully allogeneic haplotypes tested) even in the presence of interleukin 2. Reactivity to the T cell mitogen concanavalin A was, in contrast, only partially reduced. Since rat TcR1 cells are activated by concanavalin A, these results suggest that the TcR1 cells present in TcR2-suppressed rats are functional, but do not respond to foreign major histocompatibility complex antigens at a high frequency, a finding of possible importance for immunosuppression with anti-TcR2 monoclonal antibody in human allografting. Neonatally TcR2-suppressed rats were unable to respond to the strong T-dependent antigen keyhole limpet hemocyanin administered intraperitoneally in alum with B. pertussis. Thus, in the absence of peripheral TcR2 cells, the numerically expanded TcR1 T cells are not capable of providing help for B lymphocytes.
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PMID:The neonatally T cell receptor 2-suppressed rat: lymphocyte subset composition and immune reactivity. 170 19

Autoantibodies against the cardiac beta 1-adrenoceptor are present in the sera of patients with idiopathic dilated cardiomyopathy and may modulate the responsiveness of cardiac beta-adrenergic pathways to agonists. The regulation of cardiac adenylate cyclase activity by autoantibodies was examined in 50 patients with dilated cardiomyopathy. Inhibition of isoproterenol-sensitive adenylate cyclase activity could be demonstrated by serum dilutions or IgG in 52% (26 of 50) of the patients; basal and NaF-stimulated activities, in contrast, were unaffected. In 14 patients, both ligand binding to beta-receptor and isoproterenol-sensitive adenylate cyclase activity were inhibited by 100-fold serum dilutions. Pretreatment of cardiac membranes with pertussis toxin did not affect inhibition of adenylate cyclase indicating that the effect of sera does not depend on Gi. The immunogenetic control of antireceptor antibodies was examined by comparing the distribution of HLA antigens in antibody-positive and antibody-negative patients. HLA-DR4 and HLA-DR1 were strongly associated with antibodies inhibiting ligand binding and adenylate cyclase activity (71% of patients with such antibodies typed as either DR4 or DR1). Conversely 58% of patients with HLA-DR4 and 71% of patients with HLA-DR1 antibodies showed inhibition of adenylate cyclase activity compared to 46% of those who lacked both HLA-DR4 and HLA-DR1 antibodies. These results strongly suggest that cardiac beta-adrenergic receptors and adenylate cyclase activity in dilated cardiomyopathy can be modulated by circulating autoantibodies, the presence of which is under the control of the major histocompatibility complex.
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PMID:Influence of anti-beta-receptor antibodies on cardiac adenylate cyclase in patients with idiopathic dilated cardiomyopathy. 216 38

The role of cAMP in lymphocyte proliferation was investigated in the response of a monoclonal T-cell population to a specific antigen and compared to the response to interleukin-2 (IL-2) and allogeneic cells. Myelin basic protein (MBP)-reactive and encephalitogenic T-cell clones were established from long-term lines derived from SJL/J (H-2s) mice. The clone 4b.14a recognizes the peptide sequence 89-101 of the MBP molecule in association with 1-As products of the major histocompatibility complex (MHC). Incubation of 4b.14a cells with syngeneic antigen-presenting cells, previously pulsed with the 89-101 synthetic peptide or with 80 U/ml of IL-2, or allogeneic H-2Ik cells, resulted in a significant increase in the accumulation of intracellular cAMP. This increase was preceded by a peak in membranal adenylate cyclase (AC) activity. Parallel time kinetics but significantly higher cAMP production and AC activity were observed when the cells were treated with pertussis toxin. At the same concentrations the toxin inhibits cellular proliferative responses, assayed by [3H]thymidine incorporation. Our results indicate the involvement of cAMP as a positive signal in the activation of the 4b.14a clone.
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PMID:Cyclic adenosine 3',5'-monophosphate metabolism in activated T-cell clones. 247 34

A mouse model for encephalopathy induced by pertussis immunization has been described; it has features that closely resemble some of the severe reactions, including seizures and a shock-like state leading to death, occasionally seen after administration of Bordetella pertussis (whooping cough) vaccine. Susceptibility to encephalopathy maps to genes of the major histocompatibility complex and correlates as well with the genetic regulation of the level of antibody response to bovine serum albumin. In this study we have investigated which bacterial determinant is responsible for the encephalopathy. Two lines of evidence implicate pertussis toxin as the active bacterial component. Single-site mutants of B. pertussis with single affected virulence factors were tested. A mutant that produces a defective pertussis toxin had greatly diminished capacity to induce encephalopathy, whereas a hemolysin- and adenylate-cyclase-deficient avirulent mutant had the same activity in the mouse model as a virulent strain. Purified pertussis toxin plus bovine serum albumin was tested and found to induce the lethal encephalopathy, demonstrating that the toxin was the critical constituent of B. pertussis responsible for encephalopathy.
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PMID:Pertussis toxin is required for pertussis vaccine encephalopathy. 286 45

BDF1 mice were immunized with a protein antigen, such as ovalbumin (OA) or keyhole limpet hemocyanin (KLH), absorbed to aluminum hydroxide gel, and their spleen cells were stimulated by homologous antigen for the formation of glycosylation-enhancing factor (GEF). It was found that GEF obtained from OA-primed spleen cells had affinity for OA, whereas those derived from KLH-primed spleen cells had affinity for KLH. Nonspecific GEF, which was obtained by stimulation of normal spleen cells with pertussis toxin, failed to bind OA or KLH. Both antigen-specific GEF and nonspecific GEF are inactivated by phenylmethylsulfonyl fluoride, but not by N-alpha-p-tosyl-L-lysyl-chloromethyl ketone. Both factors can be partially purified by binding to p-aminobenzamidine agarose and elution with benzamidine. These findings suggest that not only non-specific GEF but also antigen-specific GEF are serine protease(s). The antigen-specific GEF consisted of two m.w. species, of 65 to 85 kilodaltons (Kd) and 40 to 55 Kd, whereas nonspecific GEF consisted of 50 to 70 Kd and 20 to 30 Kd molecules. The OA-specific GEF augmented the in vitro secondary indirect PFC response of DNP-OA-primed cells to the homologous antigen, but failed to affect the PFC response of DNP-KLH-primed cells to DNP-KLH. Similarly, KLH-specific GEF enhanced the response of DNP-KLH-primed cells but not the response of DNP-OA-primed cells. However, OA-specific GEF failed to replace the requirement for antigen-primed helper T cells. Antigen-specific GEF bound to alloantibodies reactive to the products of the I region of the major histocompatibility complex. The results collectively suggest that antigen-specific GEF is identical to antigen-specific augmenting factors described by other investigators.
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PMID:Augmentation of the antibody response by antigen-specific glycosylation-enhancing factor. 349 77

Inbred strains of mice were studied for their susceptibility to the induction of experimental allergic orchitis after sensitization with mouse testicular homogenate in complete Freund's adjuvant accompanied by injections of extract from Bordetella pertussis. Susceptibility to autoimmune orchitis was found to be linked to the major histocompatibility complex in BALB/c and C57BL/10 mice and mapped to genes encoded within the H-2Dd region. In five of six groups of bidirectional (susceptible X resistant)F1 hybrids, H-2Dd-linked susceptibility was inherited as a dominant autosomal trait. However, in (BALB/cByJ X DBA/2J)F1 and (DBA/2J X BALB/cByJ)F1 hybrids, dominant autosomal resistance to the induction of autoimmune orchitis was observed. Backcross analysis between the resistant F1 hybrid and the susceptible BALB/cByJ parent suggests that a single independently segregating DBA/2J locus is capable of negating H-2Dd-linked susceptibility, and controls resistance to the induction of autoimmune orchitis.
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PMID:Experimental allergic orchitis in mice. I. Genetic control of susceptibility and resistance to induction of autoimmune orchitis. 393 96

Anti-T-cell-line antisera were raised by repeatedly injecting mice with syngeneic, antigen-specific, delayed hypersensitivity (DH) inducing cells grown as continuous T-cell lines in vitro. Many of these antisera could induce antigen-specific DH responses which, in some cases, were rather slight. For example, the DH reaction to azobenzenearsonate induced in A/J mice by an A/J antiserum produced against the syngeneic azobenzenearsonate-specific cell line AA3 was only a weak response. Administration of pertussigen, a protein purified from Bordetella pertussis, markedly enhanced this response and prolonged its duration. Histologically the reaction showed the classical mononuclear infiltration of DH. It could be transferred to naive mice by lymph node cells that were anti-Thy-1.2 sensitive, and the transfer was restricted by genes of the major histocompatibility complex (MHC). The induction of DH by antiserum, however, was not influenced by MHC or non-MHC gene products.
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PMID:Delayed hypersensitivity induced by anti-T-cell-line antisera is enhanced by pertussigen and not restricted by histocompatibility genes. 630 Aug 89

Skin allografting was performed in rats treated with cyclosporine using strain combinations that differed across the RT1.A (class I) or RT1.B (class II) loci of the major histocompatibility complex (MHC) or across non-MHC loci. Injection of cyclosporine (20 mg/kg) for 14 consecutive days was followed by prolonged acceptance (MST = 67 days) of the skin allografts. Bordetella pertussis vaccine potentiated the effect of cyclosporine, and the synergistic effect of the vaccine occurred only when it was given before grafting. The cyclosporine given for 14 days with or without B pertussis failed to prolong second-set skin grafts. Production of hemagglutinating antibodies in cyclosporine-treated animals was completely suppressed when the skin grafts were in place, and it occurred to a much lesser extent following rejection, as compared with untreated animals. The cyclosporine did not, however, influence the antibody response following second set skin graft rejection. A system in which rats were treated for only 6 days with cyclosporine was developed in order to test the effects of disparities at different histocompatibility loci on the response to cyclosporine, because this regimen gave a marginal, but significant, prolongation of skin grafts across a full RT1 (MHC) difference. There was a differential effect of cyclosporine treatment depending upon the genetic differences involved: a skin graft across an RT1.A (class I) difference was indefinitely prolonged, one across an RT1.B (class II) or RT1.AB difference was slightly prolonged (9 to 12 days and 12.5 to 16.5 days, respectively) and a graft across non-MHC differences was not affected. Hence, the immunosuppressive effects of cyclosporine on skin graft rejection appear to depend upon the genetic disparities between donor and recipient. Exploitation of this finding may lead to the design of more effective, multidrug protocols for the treatment of rejection that would have fewer deleterious side-effects.
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PMID:Prolongation of skin graft survival across different genetic barriers in rats with cyclosporine--and its potentiation by Bordetella pertussis vaccine. 634 41


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