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Extrapituitary prolactin promoter polymorphism in Czech patients with systemic lupus erythematosus and rheumatoid arthritis
  1. Markéta Fojtíková1,
  2. Marie Černá2,
  3. Pavlína Čejková2,
  4. Šárka Růžičková3,
  5. Ctibor Dostál1
  1. 1Institute of Rheumatology, Na Slupi 4, Prague, Czech Republic
  2. 2Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles University in Prague, Prague, Czech Republic
  3. 3Department of Molecular Biology and Immunogenetics, Institute of Rheumatology, Na Slupi 4, Prague, Czech Republic
  1. Correspondence to:
    Dr M Fojtíková
    Department of Cell and Molecular Biology, Third Faculty of Medicine, Charles University in Prague, Ruská 87, 100 00 Prague 10, Czech Republic; fmar{at}centrum.cz

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Prolactin (PRL) and its production by lymphocytes have been suggested to play a distinct role in the pathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).1,2 PRL acts as a cytokine and influences the maturation and differentiation of immune cells.3,4 Extrapituitary PRL synthesis is regulated by an alternative promoter,5 which contains a single-nucleotide polymorphism (SNP) at the region −1149 G/T. Higher PRL mRNA expression is associated with the G allele in lymphocytes.6 High frequency of the G allele was described in patients with SLE,7 but was not confirmed in other work.8

We investigated −1149 G/T SNP in 156 patients with SLE and 173 patients with RA, and in 123 healthy individuals (control group). Patients …

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