Immune cell discovery could lead to better treatments for kidney disease
Monash University researchers have discovered that two types of immune cells inside blood vessels work together to cause inflammatory kidney disease, paving the way for future targeted treatments.
The discovery, published last week in the prestigious journal Proceedings of the National Academy of Sciences (USA), has shown for the first time that different types of immune cells within the blood vessels interact and send instructions to cause damage to the kidney.
Scientists from the School of Clinical Sciences at Monash Health (SCS) examined different immune cells (known as neutrophils and monocytes) in glomerulonephritis, a disease characterised by inflammation of the glomeruli.
“Glomeruli are structures in the kidney important for filtering blood and producing urine,” said lead researcher Dr Michaela Finsterbusch from the Centre for Inflammatory Diseases.
“While previous studies showed neutrophils can be responsible for causing glomerulonephritis, we’ve now discovered that another cell type, monocytes, also contribute to the disease.”
“Monocytes do this by communicating with and instructing the neutrophils—under the microscope we can see the cells actually physically interacting in the small blood vessels of the glomerulus,” said Dr Finsterbusch.
Using highly advanced microscopy techniques, the research team visualised monocytes and neutrophils in real time and saw the cells frequently interacting with each other in healthy glomeruli.
Dr Finsterbusch said that during inflammation, the duration of the interactions was prolonged and was associated with a higher degree of disease-causing neutrophil activation.
“So discovering that interactions between immune cells within the blood stream are critical for inducing injury and inflammation is really quite unusual.”
Understanding how these immune cells interact and cause disease is the next step towards developing improved treatments for patients.
“If we could control the behaviour of the monocytes, we may be able to stop them patrolling and instructing the neutrophils to cause damage, thereby dampening inflammation,” said Monash Health nephrologist and physician-scientist Professor Richard Kitching, a co-author on the study.
Currently, most available therapies for inflammatory diseases are general anti-inflammatory and immunosuppressive drugs that have undesirable side effects including increased infections, weight gain, hypertension, diabetes, cataracts and osteoporosis.
“This basic scientific discovery may lead to more targeted drugs without the unacceptable side effects both in the immune system and metabolically.”