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In vitro, prostaglandins (PG) have strong inhibitory effects on T cell activation and proliferation and inhibitors of PG synthesis (NSAID) increase proliferation and activation of T cells. Although most studies have failed to demonstrate cyclooxygenase (COX) activity in lymphocytes, there is contradictory evidence on the synthesis of different PG. We have studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot the expression of COX-1 and -2 mRNA and protein in resting and activated peripheral blood or Jurkat T cells. Cells were activated by T cell receptor triggering with OKT3 antibodies and activation confirmed by flow cytometric analysis of surface CD69. COX enzymatic activity was measured by determination of arachidonic acid (AA)-induced PG synthesis. Both peripheral blood and Jurkat T cells expressed COX-1 and -2 mRNA and protein. COX-1 was constitutively expressed and did not change after OKT3 stimulation. COX-2 was inducible upon OKT3-induced activation. In spite of the presence of COX mRNA and immunoreactive protein, AA-induced PG synthesis was not detected at the EIA detection (pM) level. The potential role of cyclooxygenases in T cells deserves further study, since no PG of the studied series seem to be synthesized by T cells.

Objective: To investigate the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in cells from synovial fluid (SF) of patients with acute or chronic arthritis., Methods: SF was obtained from eight patients with acute crystal-induced arthritis, nine with rheumatoid arthritis and four with psoriatic arthritis. COX-1 and COX-2 gene expression was studied by reverse transcriptase-polymerase chain reaction (RT-PCR). Protein expression was detected by Western blotting and immunocytochemistry., Results: There was expression of COX-1 mRNA in all and COX-2 mRNA in most of the SF samples from acute or chronic arthritis. By immunocytochemistry, both COX-1 and COX-2 immunoreactivity was restricted to a variable fraction of mononuclear cells. COX-1 staining was observed in 10-fold more cells than COX-2. By Western blotting, COX-1 protein was detected in 60% of the SF samples and COX-2 in none. There were no differences in the pattern of COX-1 and COX-2 expression between chronic and acute SF samples., Conclusion: In arthritis, both COX-1 and COX-2 isoforms are expressed by SF cells. COX-1 is the most abundant isoform. Since the strong COX-1 immunostaining observed in a fraction of mononuclear SF cells is not observed in peripheral blood leucocytes, it may be the result of either the activation or recruitment of a subset of mononuclear cells with a high COX-1 expression level.

We investigate whether a heat-shock protein gene (HSP70-2) is involved in determining susceptibility to systemic lupus erythematosus (SLE) in a Spanish population. A HSP70-2 PstI polymorphism was characterized by restriction fragment length polymorphism analysis of polymerase chain reaction-amplified genomic DNA in 90 SLE patients and 117 controls. The PstI site containing allele (B) was significantly increased in SLE patients compared to healthy controls. This was due to a significant increase in the BB homozygous genotype in patients, particularly in those with diffuse proliferative nephritis. Neither allelic nor genotypic differences were detected when compared by the presence or absence of DR3. The HSP70-2 B allele seems tightly linked to the human leucocyte antigen (HLA) haplotypes carrying susceptibility to SLE in our population. An independent role for this gene cannot be confirmed due to its linkage with HLA DR3.

We have studied the skin and nerve fibrosis in toxic oil syndrome by in situ hybridization using specific cDNA probes for types I, III, and IV collagens. Fibroblasts with high levels of type I and III collagen mRNA were observed in biopsies from fibrotic skin areas. Similarly, type IV collagen mRNA was abundant in cells within the fibrotic process of the nerves. These results suggest that the excessive accumulation of collagen in toxic oil syndrome results from transcriptional activation of collagen genes in a subpopulation of fibroblasts.