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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

C1q and C3 in bronchoalveolar lavage fluid from patients with summer-type hypersensitivity pneumonitis.

Immune complexes have been thought to participate in the pathogenesis of hypersensitivity pneumonitis, but the role of complement components is not defined. In our study of nine patients with summer-type hypersensitivity pneumonitis (summer-type HP), C1q in bronchoalveolar lavage fluid (BALF) was strikingly increased (mean 3.7, range 0.4 to 10 micrograms/ml). The value of C1q/albumin was several to 20 times greater in BALF than in serum samples from individual patients. In contrast, BALF samples from control subjects (ten patients with sarcoidosis and nine normal subjects) contained an undetectable amount (less than 0.02 micrograms/ml) of C1q. C3 in BALF also increased in the summer-type HP patients. Furthermore, C1q (as well as specific IgG and IgA antibody activities to Trichosporon cutaneum antigen) in BALF correlated with clinical symptoms and diffusing capacity (DCO), while the BAL lymphocytosis or the change of OKT4/OKT8 ratio did not. These findings are indicative of local secretion or concentration mechanism of C1q and C3, supporting the involvement of immune complexes in the respiratory tract of the patients.[1]

References

  1. C1q and C3 in bronchoalveolar lavage fluid from patients with summer-type hypersensitivity pneumonitis. Soda, K., Ando, M., Sakata, T., Sugimoto, M., Nakashima, H., Araki, S. Chest (1988) [Pubmed]
 
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