This study provides the first evidence of extrahepatic synthesis of C-reactive protein by human peripheral blood lymphocytes, specifically large granular lymphocytes/NK effectors.
Challenges hepatic exclusivity of CRP synthesis; leaves open its clinical relevance pending human validation.
Biosynthetic labeling with [35S]met and immunoprecipitation with anti-C-reactive protein (CRP) antibodies and Staphylococcus aureus indicate that cell surface CRP is produced by lymphocytes. The ability of anti-CRP to reduce NK activity, and the demonstration that 125I-anti-CRP-labeled PBL are found in low-density Percoll fractions associated with large granular lymphocyte (LGL) and NK activity suggest that S-CRP-bearing cells are NK effectors. The production of S-CRP by LGL supports this hypothesis. While lymphocytes were shown to synthesize S-CRP, monocytes produced no detectable S-CRP. The lymphocytes that produce S-CRP apparently do not secrete it; when lymphocyte culture supernatants were tested, no S-CRP was found. This is the first description of extrahepatic synthesis of CRP.
No takes yet. Share an insight, caveat, or question.
Kuta et al. (1986) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: