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4 Accelerated lupus nephritis associated with increased t helper subset, serum tnfa and anti dsdna levels in pregnant pristane induced lupus mice
  1. N Nurdiana1,
  2. U Kalsum1,
  3. E Sari Dewi2,
  4. K Handono3 and
  5. H Kaliim4
  1. 1Brawijaya University, Clinical Pharmacology, Malang, Indonesia
  2. 2Brawijaya University, Nursery, Malang, Indonesia
  3. 3Brawijaya University, Clinical pathology, Malang, Indonesia
  4. 4Brawijaya University, Rheumato-Immunology Division- Internal medicine, Malang, Indonesia

Abstract

Background and aims To investigate the role of T helper (Th) cell subsets and TNFα in the pathogenesis of nephritis in pregnant SLE mice model.

Methods Thirty female Balb/c mice were divided into two groups: non-pregnant and pregnant lupus mice . SLE induction was done by single intraperitoneal injection of 0.5 cc pristane. After twelve weeks post injection, mice were mated. Periodically, blood pressure was monitored and urine albumin level was measured by ELISA. After 18 day, mice were euthanized, and renal biopsy was done to evaluate the development of nephritis. Placental TNFα and serum anti-dsDNA were measured by ELISA. Spleen Th1, Th2, and Th17 percentages were measured by flowcytometry

Results Th1, Th2, and Th17 percentages in were significantly higher in pregnant lupus mice compared to non pregnant group. Th1 and Th17 percentages were positively correlated with albuminuria, anti-dsDNA, systolic, and diastolic blood pressure. Incidence of lupus nephritis was higher in pregnant lupus mice with higher activity index compared to non pregnant mice. The activity index also had positive correlations with Th1 and Th2 percentages. Higher placental TNFα and anti-dsDNA levels were found in pregnant lupus mice. Placental TNFα and anti-dsDNA levels were positively correlated with albuminuria. Moreover, placental TNFα levels were positively correlated with systolic and diastolic blood pressure.

Conclusions High percentages of Th cell subsets, TNF α and anti ds DNA antibody were associated with renal disorder in pregnant lupus mice which propose a new mechanism for the pregnancy complication in SLE.

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