Related Experiment Video
Updated: Aug 14, 2026
Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
Published on: December 26, 2017
Macrophage migration inhibitory factor contributes to anti-neutrophil cytoplasmic antibody-induced neutrophils
Jian Hao1, Tie-Gang Lv1, Chen Wang2
1Renal Division, Department of Medicine, The Affiliated Hospital of Inner Mongolia Medical College, Huhehot, Inner Mongolia 010050, China.
Background:
Macrophage migration inhibitory factor (MIF) is an inflammatory mediator released by macrophages that is central to the innate immune system, with an upstream role in the inflammatory cascade. MIF is one of the most important pathogenic factors in the development of the autoimmune diseases. In the current study, we investigated the role of MIF in anti-neutrophil cytoplasmic antibody (ANCA)-induced neutrophil activation.
Methods:
Plasma levels of MIF from 31 patients with active ANCA-associated vasculitis (AAV) were analyzed by ELISA. The various effects of MIF in ANCA-induced neutrophil respiratory burst and degranulation were measured.
Results:
Plasma levels of circulating MIF were significantly higher in AAV patients with active disease compared with those in remission and healthy controls. Compared with MIF-primed neutrophils, the MFI value increased significantly in MIF-primed neutrophils further activated with MPO-ANCA-positive IgG or PR3-ANCA-positive IgG (270.8±9.7 vs. 421.5±9.7, P<0.001; 270.8±9.7 vs. 414.1±15.6, P<0.001, respectively). Compared with MIF-primed neutrophils, the lactoferrin concentration increased significantly in the supernatant of MIF-primed neutrophils further activated by MPO-ANCA-positive IgG (567.8±61.2ng/ml vs. 1677.0±42.5ng/ml, P<0.001) or PR3-ANCA-positive IgG (567.8±61.2ng/ml vs. 1546.0±116.2ng/ml, P<0.001), respectively. Interleukin-8 (IL-8), IL-6 and IL-23 were involved in ANCA-induced activation of MIF-primed neutrophils.
Conclusions:
MIF primes neutrophils by increasing ANCA antigen translocation. The primed neutrophils can be further induced by ANCA, resulting in respiratory burst and degranulation.
Insights
Macrophage migration inhibitory factor (MIF) primes neutrophils, increasing their activation by anti-neutrophil cytoplasmic antibodies (ANCA). Elevated MIF levels are observed in active ANCA-associated vasculitis, indicating its role in autoimmune disease pathogenesis.
Area of Science:
- Immunology
- Autoimmune Diseases
- Inflammation
Background:
- Macrophage migration inhibitory factor (MIF) is a key inflammatory mediator in innate immunity and a significant factor in autoimmune disease development.
- This study investigates the role of MIF in the activation of neutrophils by anti-neutrophil cytoplasmic antibodies (ANCA).
Purpose of the Study:
- To elucidate the role of MIF in ANCA-induced neutrophil activation.
- To determine the correlation between MIF levels and active ANCA-associated vasculitis (AAV).
Main Methods:
- Plasma MIF levels were quantified using ELISA in 31 patients with active AAV, remission, and healthy controls.
- The impact of MIF on ANCA-induced neutrophil respiratory burst and degranulation was assessed.
Main Results:
- Circulating MIF levels were significantly elevated in AAV patients with active disease compared to those in remission and healthy individuals.
- MIF-primed neutrophils showed significantly increased activation, respiratory burst, and degranulation when further stimulated with MPO-ANCA or PR3-ANCA IgG.
- Interleukin-8 (IL-8), IL-6, and IL-23 were identified as key cytokines involved in ANCA-induced activation of MIF-primed neutrophils.
Conclusions:
- MIF primes neutrophils by enhancing ANCA antigen translocation, making them more susceptible to activation.
- Primed neutrophils, upon further induction by ANCA, exhibit increased respiratory burst and degranulation, contributing to vasculitis pathogenesis.
