| 1. |
|
|
| 2. |
|
|
| 3. |
- Ronmark, E, et al.
(författare)
-
Asthma among children in a dry climate.
- 1998
-
Ingår i: JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. - 0091-6749. ; 101:1, s. S181-S181
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)
|
|
| 4. |
- Ryan, M, et al.
(författare)
-
Bordetella pertussis respiratory infection in children is associated with preferential activation of type 1 T helper cells.
- 1997
-
Ingår i: Journal of Infectious Diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 175:5, s. 1246-50
-
Tidskriftsartikel (refereegranskat)abstract
- The mechanism of protective immunity against Bordetella pertussis generated following recovery from whooping cough in childhood has not yet been elucidated. Studies with a murine respiratory infection model have indicated that cellular immunity, mediated by Th1 cells, plays a role in the clearance of a primary infection with B. pertussis and in protection against subsequent challenge. In the present study, the induction of B. pertussis-specific Th cell subsets in children was examined. Peripheral blood mononuclear cells from B. pertussis-infected or convalescent children proliferated and secreted cytokines following antigen stimulation in vitro. In contrast, responses were weak or undetectable in the majority of children who had not been infected or vaccinated. In all cases, responding T cells produced interferon-gamma but low or undetectable interleukin-5. The findings suggest that Th1 cells may play a role in protective immunity generated following infection with B. pertussis in children.
|
|
| 5. |
- Ryan, M, et al.
(författare)
-
Bordetella pertussis-specific Th1/Th2 cells generated following respiratory infection or immunization with an acellular vaccine : comparison of the T cell cytokine profiles in infants and mice.
- 1997
-
Ingår i: Developments in biological standardization. - 0301-5149. ; 89, s. 297-305
-
Tidskriftsartikel (refereegranskat)abstract
- In an investigation of cell-mediated immunity against Bordetella pertussis, we found that B. pertussis infection in infants and in mice was associated with the induction of antigen-specific T cells that secrete IFN-g and IL-2, but not IL-4 or IL-5. This cytokine profile is characteristic of Th1 cells that mediate cellular immune responses against a range of intracellular pathogens. An examination of cytokine production following immunization with a three-component acellular vaccine, comprising inactive PT, FHA and pertactin adsorbed to alum, demonstrated that spleen cells from vaccinated mice produced high levels of IL-5, but no detectable IFN-g and low levels of IL-2. In contrast, peripheral blood mononuclear cells from vaccinated infants produced IL-2, IL-5 and IFN-g. These findings highlight significant differences in the immune responses generated by vaccination and natural infection with B. pertussis and demonstrate that the T-cell response induced with an acellular vaccine, although dominated by type 2 cytokines in mice, is more heterogeneous in infants with a Th0 or mixed Th1/Th2 cytokine profile.
|
|
| 6. |
- Ryan, M, et al.
(författare)
-
Distinct T-cell subtypes induced with whole cell and acellular pertussis vaccines in children.
- 1998
-
Ingår i: Immunology. - : Wiley. - 0019-2805 .- 1365-2567. ; 93:1, s. 1-10
-
Tidskriftsartikel (refereegranskat)abstract
- Recent clinical trials have demonstrated that new generation acellular pertussis vaccines can confer protection against whooping cough. However, the mechanism of protective immunity against Bordetella pertussis infection induced by vaccination remains to be defined. We have examined cellular immune responses in children immunized with a range of acellular and whole cell pertussis vaccines. Immunization of children with a potent whole-cell vaccine induced B. pertussis-specific T cells that secreted interferon-gamma (IFN-gamma), but not interleukin-5 (IL-5). In contrast, T cells from children immunized with acellular pertussis vaccines secreted IFN-gamma and/or IL-5 following stimulation with B. pertussis antigens in vitro. These observations suggest that protective immunity conferred by whole-cell vaccines, like natural immunity, is mediated by type 1 T cells, whereas the mechanism of immune protection generated with acellular vaccines may be more heterogeneous, involving T cells that secreted type 1 and type 2 cytokines.
|
|
| 7. |
- Wilson, Sara I, et al.
(författare)
-
Escape mutants of HIV-1 proteinase : enzymic efficiency and susceptibility to inhibition
- 1997
-
Ingår i: Biochimica et Biophysica Acta. - 0006-3002 .- 1878-2434. ; 1339:1, s. 113-125
-
Tidskriftsartikel (refereegranskat)abstract
- Genes encoding a number of mutants of HIV-1 proteinase were sub-cloned and expressed in E. coli. The proteinases containing mutations of single residues (e.g., G48V, V82F, I84V and L90M) were purified and their catalytic efficiencies relative to that of wild-type proteinase were examined using a polyprotein (recombinant HIV-1 gag) substrate and several series of synthetic peptides based on the -Hydrophobic * Hydrophobic-, -Aromatic * Pro- and pseudo-symmetrical types of cleavage junction. The L90M proteinase showed only small changes, whereas the activity of the other mutant enzymes was compromised more severely, particularly towards substrates of the -Aromatic * Pro- and pseudo-symmetrical types. The susceptibility of the mutants and the wild-type proteinase to inhibition by eleven different compounds was compared. The L90M proteinase again showed only marginal changes in its susceptibility to all except one of the inhibitors examined. The K(i) values determined for one inhibitor (Ro31-8959) showed that its potency towards the V82F, L90M, I84V and G48V mutant proteinases respectively was 2-, 3-, 17- and 27-fold less than against the wild-type proteinase. Several of the other inhibitors examined form a systematic series with Ro31-8959. The inhibition constants derived with these and a number of other inhibitors, including ABT-538 and L-735,524, are used in conjunction with the data on enzymic efficiency to assess whether each mutation in the proteinase confers an advantage for viral replication in the presence of any given inhibitor.
|
|
| 8. |
|
|
