COX-2 inhibitors can down-regulate in vivo antibody response against T-dependent antigens

Roum Arch Microbiol Immunol. 2006 Jan-Jun;65(1-2):59-65.

Abstract

There are many studies demonstrating by different experimental models that non-steroidal antiinflammatory drugs (NSAIDs), also known as cyclooxygenase-2 (COX-2) inhibitors, can modulate immune response such as lymphoid cells differentiation and proliferation. There are experimental data which show that activated B cells can express mRNA COX-2, release prostaglandins (PGs) and produce immunoglobulins in PGs dependent manner. In this study, using different COX-2 inhibitors and applying personalized immunization scheme, we confirmed that it is possible to modulate in vivo antibody response against T cell dependent antigens, substantiating the importance of PGE2 and E prostanoid receptor (EP-R) in antibody generation. Our results point out the fact that we must be more careful when we apply vaccines containing T-cell dependent antigens, such as tetanus or diphteric anatoxin, to the patients under an intense antiinflammatory treatment.

MeSH terms

  • Animals
  • Antibodies, Bacterial / biosynthesis*
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Dinoprostone / metabolism
  • Diphtheria Toxin / immunology*
  • Diphtheria Toxin / metabolism
  • Freund's Adjuvant
  • Immunization, Secondary
  • Lipopolysaccharides / immunology
  • Male
  • Mice
  • T-Lymphocytes / immunology*
  • Tetanus Toxin / immunology*
  • Tetanus Toxin / metabolism
  • Tetanus Toxoid / immunology*
  • Toll-Like Receptor 2 / immunology
  • Toll-Like Receptor 2 / metabolism
  • Toll-Like Receptor 4 / immunology
  • Toll-Like Receptor 4 / metabolism

Substances

  • Antibodies, Bacterial
  • Cyclooxygenase 2 Inhibitors
  • Diphtheria Toxin
  • Lipopolysaccharides
  • Tetanus Toxin
  • Tetanus Toxoid
  • Toll-Like Receptor 2
  • Toll-Like Receptor 4
  • Freund's Adjuvant
  • Dinoprostone