Treatment with infliximab was well tolerated and caused a decrease in the number of patients with exacerbations in symptomatic moderate asthma. The promising preliminary findings underscore the need to evaluate therapy directed against TNF-alpha in larger trials enrolling patients with more severe asthma.
Recombinant adenoassociated virus (rAAV) type 2 vectors have been used to transduce a wide variety of cell types, including hematopoietic progenitor cells. For in vivo gene transfer, it is desirable to have an rAAV vector that specifically transduces selected target cells. As a first step toward generating an rAAV vector capable of targeting delivery in vivo, we have engineered a chimeric protein combining the AAV capsid protein and the variable region of a single-chain antibody against human CD34 molecules, a cell surface marker for hematopoietic stem/progenitor cells. Inclusion of the chimeric CD34 single-chain antibody-AAV capsid proteins within an rAAV virion significantly increased the preferential infectivity of rAAV for the CD34+ human myoleukemia cell line KG-1, which is normally refractory to rAAV transduction. Antibodies against the single-chain antibody and the CD34 protein blocked this transduction. This chimeric vector represents a significant improvement in the host range of rAAV and the first step toward specific gene delivery by rAAV vectors to cells of choice, in this case, hematopoietic progenitor cells, for the treatment of human disease.
In this pilot safety study of 48 patients with mild or moderate asthma who had bronchial reactivity to adenosine monophosphate, regadenoson was safe and well tolerated.
Setipiprant at multiple oral doses was well tolerated and reduced both the allergen-induced LAR and the associated AHR in allergic asthmatics. Our findings confirm that CRTH2 may be a promising target for the treatment of allergic disorders.
Circulating antibodies to myeloperoxidase (MPO) have been described in a variety of vasculitic syndromes, drug-induced SLE and drug-induced nephritis. We have examined the autoantibody profile in acute sera from patients with antineutrophil cytoplasmic antibody-positive vasculitis (n = 8), drug-induced nephritis (n = 4), drug-induced lupus (n = 7), SLE (n = 27) and nephritis-associated with SLE (n = 17). Significant binding to purified MPO in ELISA was given by all sera from patients with vasculitis and drug-induced nephritis but ANA sought by indirect immunofluorescence on HEp-2 cells were not detected. Both anti-MPO and ANA were found in sera from patients with drug-induced lupus. Sera from patients with SLE or SLE nephritis did not contain high titres of anti-MPO antibodies but invariably contained ANA. Anti-MPO antibodies of both IgG and IgM classes were present in all sera from patients with drug-induced disease. Although the number of samples tested was small, sera from patients with drug-induced nephritis showed significantly greater median % binding of IgM to MPO compared with drug-induced SLE. Binding to MPO by IgG in these sera was not significantly different. These findings suggest that the mechanism of interaction between hydralazine and the immune system in the two drug-induced autoimmune diseases studied may contribute to their distinct clinical features.
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