Guidance and Resources for Those with Axial Spondyloarthritis

Axial spondyloarthritis (AxSpA) encompasses a group of inflammatory arthritis conditions primarily impacting the spine, though other joints and even organs can be involved. We invite you to discover more about this range of conditions, their diagnosis and treatment options, and ways you can manage them effectively.

Living with axial spondyloarthritis (AxSpA) presents daily hurdles. There are two main types: radiographic axSpA, also known as ankylosing spondylitis, visible on X-rays due to damage to the sacroiliac joints and spine, and nonradiographic axSpA (nr-axSpA) which might not show on X-rays but can be detected through MRIs. We're here to guide you with expert advice, resources, and support to navigate through your AxSpA journey and alleviate its symptoms.

New Discovery in Immune Cell Regulation: What It Means for Arthritis and Inflammation

New Discovery in Immune Cell Regulation: What It Means for Arthritis and Inflammation

August 22, 20243 min read

A recent discovery from the University of Exeter’s MRC Centre for Medical Mycology has the potential to revolutionize how we treat inflammatory diseases like rheumatoid arthritis, lupus, and even severe COVID-19. This exciting research, published in Nature, explores how a special receptor called MICL (myeloid inhibitory C-type lectin) plays a key role in controlling inflammation, potentially paving the way for new therapies.

What is the MICL Receptor and Why Is It Important?

Our immune system is a complex network of cells and signals designed to protect us from infections and repair tissue damage. However, when this system goes into overdrive, it can cause chronic inflammation, which leads to damage in healthy tissues. In diseases like rheumatoid arthritis, this means joint pain, swelling, and long-term damage. Finding ways to balance this immune response is a crucial goal in developing better treatments.

MICL acts like a “brake” in the immune system. While most receptors on immune cells tell them to attack when there’s a threat, MICL does the opposite. It helps prevent over-activation of the immune response, ensuring that the body doesn’t go into full inflammation mode when it’s not necessary. Lead researcher Dr. Mariano Malamud explains that MICL could be a key to developing therapies that reduce inflammation without compromising the immune system's ability to fight infections.

MICL and Its Role in Inflammatory Diseases

One of the most exciting findings in this study is how MICL impacts neutrophils, which are the most common type of white blood cell. Neutrophils are a vital part of our immune system, rushing to the scene of an infection or injury to help defend the body. However, these cells can also undergo a process called NETosis, a form of programmed cell death. While NETosis helps fight infections, it’s also highly inflammatory.

In diseases like rheumatoid arthritis and lupus, too much NETosis can make inflammation worse. The Exeter team discovered that MICL can sense when neutrophils are undergoing NETosis and helps prevent unnecessary cell death, reducing the overall inflammatory response. This regulation is crucial because unchecked inflammation can lead to significant tissue damage, which is why targeting MICL could be so important in treating these diseases.

What This Means for People with Arthritis

For those living with rheumatoid arthritis, where inflammation is a primary driver of joint damage and pain, this discovery offers hope for new treatments. In the study, mice without MICL showed much more severe arthritis due to excessive inflammation. When MICL’s function was restored, the inflammation decreased, leading to milder disease symptoms.

What’s particularly exciting about these findings is that they suggest targeting MICL could help control the body’s inflammatory response without completely shutting down its ability to fight infections. This balance is key in developing therapies for autoimmune diseases, where the immune system mistakenly attacks healthy tissues.

A New Approach to Treating Severe COVID-19 and Other Diseases

While the focus of this research is primarily on inflammatory diseases like rheumatoid arthritis, the potential applications extend beyond that. Severe cases of COVID-19 are often marked by an out-of-control immune response, leading to excessive inflammation in the lungs and other tissues. By targeting MICL, it may be possible to manage this inflammatory response, offering better outcomes for patients with severe COVID-19 and other inflammation-related conditions.

Professor Gordon Brown, one of the senior researchers on the project, highlighted the importance of this discovery: “This breakthrough is exciting because it offers a new way to think about managing inflammation. By understanding how MICL regulates the immune system, we can begin developing therapies that address the root causes of diseases like arthritis and severe COVID-19.”

Looking Forward: The Future of Arthritis Treatments

For people with rheumatoid arthritis, this discovery is a promising step forward. Targeting MICL could offer a way to better manage inflammation, reducing pain and joint damage while allowing the immune system to continue its vital work of defending the body. While this research is still in its early stages, it provides a strong foundation for the development of new therapies.

MICL receptorRheumatoid arthritis treatmentInflammation control in autoimmune diseasesNeutrophil cell death (NETosis)Immune cell regulationAutoimmune disease therapiesSevere COVID-19 treatmentChronic inflammation solutionsNew arthritis treatmentsImmune system research breakthroughs
Back to Blog

Learn more about Arthritis:

Arthritis Advice

Get better control of your arthritis with help from our experts. Arthritis can be confusing, but don't worry, we have the tips you need to make it easier to manage.

Proud Member of the Society for Nonprofits

Have a question?

We're Here to Help

By providing my phone number, I agree to receive text messages from the business.

Copyright © 2024 American Arthritis Foundation, a qualified 501(c)(3) EIN 87-4004425, All rights reserved.