Effects of prostaglandin synthesis inhibition on the immune response.
Inhibition of prostaglandin synthesis at the time of antigen presentation was used to test the role of prostaglandins in the inductive stage of the in vivo immune response to several antigens. Indomethacin and Ro 20-5720, two prostaglandin synthesis inhibitors, produced a several-fold enhancement of the primary immunoglobulin (Ig) M and IgG anti-sheep red blood cell plaque-forming cell (PFC) response in CAF1 mice. Indomethacin and Ro 20-5720 also enhanced the antibody response to chicken serum albumin (CSA) in buffered saline. However, the antibody response to CSA in Freund's adjuvant was reduced by indomethacin treatment. Indomethacin treatment enhanced the PFC response to a chicken lysozyme-lipopolysaccharide conjugate, and did not greatly affect the PFC response to pneumococcal polysaccharide. The allogeneic cytotoxic response to the El-4 tumor line was delayed by indomethacin treatment and, since this tumor does not synthesize prostaglandins, we speculate that prostaglandin synthesis by the host is important in the generation of a cytotoxic response to this tumor. It is concluded that the role of prostaglandins in the induction of the immune response varies, and can be proinductive or anti-inductive, depending on the eliciting antigen.[1]References
- Effects of prostaglandin synthesis inhibition on the immune response. Schleimer, R.P., Benjamini, E. Immunopharmacology (1981) [Pubmed]
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