None of the patients appeared to have experienced any unusual vaccine reactions despite the fact that the pediatric formulation contains greater amounts of the detoxified pertussis toxin and diphtheria toxoid.
12.
Other scientists have developed techniques for using melanophores as biosensors, and for rapid disease detection ( based on the discovery that pertussis toxin blocks pigment aggregation in fish melanophores ).
13.
"B . bronchiseptica " does not express pertussis toxin, which is one of the characteristic virulence factors of " B . pertussis ", but it has the genes to do so, highlighting the close evolutionary relationship between the two species .,
14.
After their B subunit binds to receptors on the cell surface, the toxin is enveloped by the cell and transported inside either through The mechanism pathways for the four AB5 toxins : cholera toxin, pertussis toxin, shiga toxin, and subtilase cytotoxin.
15.
The addition of anti-CD40 causes the B cells to resemble those found in the GC . Pertussis toxin is known to inhbibit the action of G proteins and B cells treated with the toxin were observed to migrate poorly in response to FDC-SP.
16.
Briefly, they cloned the pertussis toxin, mapped the antigenic epitopes using antibodies from individuals, who had the disease and or were vaccinated with the old whole-cell vaccine, and attached these antigenic peptides onto the diphtheria toxin as a carrier and adjuvant in one.
17.
Serology may be used for adults and adolescents who have already been infected for several weeks to determine whether antibody against pertussis toxin or another virulence factor of " B . pertussis " is present at high levels in the blood of the person.
18.
The pertussis toxin ( also an AB 5 protein ) produced by " Bordetella pertussis " acts in a similar manner with the exception that it ADP-ribosylates the G? " i " subunit, rendering it inactive and unable to inhibit adenylyl cyclase production of cAMP ( leading to constitutive production ).
19.
The toxin, known as pertussis toxin ( or PTx ), inhibits G protein coupling that regulates an adenylate cyclase-mediated conversion of ATP to cyclic AMP . The end result is phagocytes convert too much ATP to cyclic AMP, which can cause disturbances in cellular signaling mechanisms, and prevent phagocytes from correctly responding to an infection.
