ArticleInflammation2012
Polarization toward Th1-type response in active, but not in inactive, lupus inhibits late allergic rhinitis in lupus-prone female NZB×NZWF(1) mice.
Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- The pathologic and clinical intersection of atopic and autoimmune disease.Current allergy and asthma reports · 2012Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The association of allergic diseases and disease activity in systemic lupus erythematosus (SLE, lupus) is controversial. The study investigates lupus activity-related differences in the induction of late allergic rhinitis (LAR) in the female NZB×NZW(B/W)F(1) mouse model for lupus. The LAR, which is induced by ovalbumin, was examined during the preactive (before clinical onset) and active (after clinical onset) phases in mice. Induction of LAR was less severe in mice with active lupus in contrast to clinically healthy lupus mice that developed a more severe allergic rhinitis. Inhibition of the development of LAR may be due to reduced eosinophilia and local interleukin-4 secretion during active autoimmune disease. In addition, systemic interferon-γ, but not IL-4, production increased during the active phase, but not the preactive phase. This suggests that the predominating Th1 lineage commitment in mice with active lupus may be responsible for the inhibition of the allergic Th2 response. The present study may shed some light on the controversy of the prevalence of allergic diseases in SLE patients.
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