Abstract

Evaluating the activity of the complement system under conditions of altered thyroid hormone levels might help elucidate the role of complement in triggering autoimmune processes. Here, we investigated alternative pathway (AP) activity in male Wistar rats (180 ± 10 g) after altering their thyroid hormone levels by treatment with triiodothyronine (T3), propylthiouracil (PTU) or thyroidectomy. T3 and thyroxine (T4) levels were determined by chemiluminescence assays. Hemolytic assays were performed to evaluate the lytic activity of the AP. Factor B activity was evaluated using factor B-deficient serum. An anti-human factor B antibody was used to measure factor B levels in serum by radial immunodiffusion. T3 measurements in thyroidectomized animals or animals treated with PTU demonstrated a significant reduction in hormone levels compared to control. The results showed a reduction in AP lytic activity in rats treated with increasing amounts of T3 (1, 10, or 50 µg). Factor B activity was also decreased in the sera of hyperthyroid rats treated with 1 to 50 µg T3. Additionally, treating rats with 25 µg T3 significantly increased factor B levels in their sera (P < 0.01). In contrast, increased factor B concentration and activity (32%) were observed in hypothyroid rats. We conclude that alterations in thyroid hormone levels affect the activity of the AP and factor B, which may in turn affect the roles of AP and factor B in antibody production.

Highlights

  • Complement consists of a group of serum and membrane proteins that protect the organism against pathogens and modified-self components, functioning as a dangersensing and transmission system [1] in innate and adaptive immune responses

  • Evaluation of complement alternative pathway (AP) activity A hemolytic assay measuring the kinetics of lysis [17,18]

  • The AP lytic activity was restored by the addition of purified human factor B, showing that we efficiently produced RB samples by heating the serum to 56°C for 180 s (Figure 2B)

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Summary

Introduction

Complement consists of a group of serum and membrane proteins that protect the organism against pathogens and modified-self components, functioning as a dangersensing and transmission system [1] in innate and adaptive immune responses. Studies evaluating complement activity in both normal physiological conditions and under conditions of altered levels of thyroid hormones might further our understanding of the role played by the CS in triggering autoimmune processes. As expected, treating rats with T3 (25 μg) for 12 days mixture was subsequently incubated at 37°C to measure (Figure 1A) increased the serum level of this hormone.

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