Division of Rheumatology, Department of Internal Medicine, and Clinical Autoimmunity Center of Excellence, University of Michigan, Ann Arbor, Michigan, USA.
Megan N Mattichak studies the mechanisms behind inflammatory arthritis, particularly how certain proteins interact with the immune system. One significant area of her research involves a protein known as CD13, which can leak into the bloodstream and trigger joint inflammation. By examining how CD13 activates the bradykinin receptor (B1R) in immune and joint cells, she seeks to understand how this process contributes to conditions like rheumatoid arthritis and explores methods to block this receptor to reduce inflammation. This research could lead to new treatments that specifically target the underlying causes of arthritis without suppressing the overall immune response.
Key findings
CD13 protein activation leads to increased activity of the bradykinin receptor (B1R), which is overactive in rheumatoid arthritis patients.
Blocking the B1R receptor reduced inflammation in human tissue samples and mouse models of arthritis.
Identifying B1R as a drug target could lead to treatments for both rheumatoid arthritis and other inflammatory diseases.
Frequently asked questions
Does Dr. Mattichak study rheumatoid arthritis?
Yes, Dr. Mattichak's work specifically focuses on rheumatoid arthritis and the mechanisms that lead to inflammation in this condition.
What treatments has Dr. Mattichak researched?
She is researching potential treatments that involve blocking the bradykinin receptor B1R to reduce inflammation caused by proteins like CD13.
Is Dr. Mattichak's work relevant to patients with inflammatory diseases?
Absolutely, her research aims to develop new therapies that could benefit patients suffering from inflammatory diseases, including rheumatoid arthritis.
Publications in plain English
Targeting CD13/Aminopeptidase N as a Novel Therapeutic Approach for Scleroderma Fibrosis.
2025
Arthritis & rheumatology (Hoboken, N.J.)
Muraoka S, Brodie WD, Mattichak MN, Gurrea-Rubio M, Ikari Y +22 more
Plain English This study focused on a condition called systemic sclerosis (SSc), an autoimmune disease that leads to thickening and scarring of the skin. Researchers found that certain proteins (CD13 and B1 receptor) were more active in the skin of patients with a severe form of SSc, contributing to excessive scar formation. By blocking the B1 receptor, they were able to reduce the fibrosis-related responses in lab tests and in mice, showing that this approach could be a new way to treat SSc.
Who this helps: This helps patients with systemic sclerosis and their doctors by potentially offering a new treatment option.
Soluble CD13 is a potential mediator of neutrophil-induced thrombogenic inflammation in SARS-CoV-2 infection.
2025
JCI insight
Tsou PS, Ali RA, Lu C, Sule G, Carmona-Rivera C +41 more
Plain English This study looked at a substance called soluble CD13 (sCD13), which is produced during COVID-19 infections. Researchers found that patients with severe COVID-19 had much higher levels of sCD13, and this was linked to increased inflammation and complications. Specifically, elevated sCD13 levels were associated with heightened immune response processes that lead to blood vessel stress and clot formation.
Who this helps: This research benefits COVID-19 patients and doctors by highlighting possible targets for new treatments.
Single-cell sequencing reveals Hippo signaling as a driver of fibrosis in hidradenitis suppurativa.
2024
The Journal of clinical investigation
van Straalen KR, Ma F, Tsou PS, Plazyo O, Gharaee-Kermani M +25 more
Plain English This study focused on hidradenitis suppurativa (HS), a long-term skin condition that leads to painful lumps and scarring. Researchers discovered that certain types of skin cells, specifically two types of fibroblasts, play a significant role in HS and found that a signaling pathway called Hippo contributes to the excessive scarring seen in patients. By blocking the Hippo pathway, they showed that it may be possible to reduce fibrosis in HS, which could lead to new treatment options.
Who this helps: This benefits patients with hidradenitis suppurativa seeking better treatment for their condition.
Activation of cytotoxic lymphocytes through CD6 enhances killing of cancer cells.
2024
Cancer immunology, immunotherapy : CII
Gurrea-Rubio M, Wu Q, Amin MA, Tsou PS, Campbell PL +14 more
Plain English This study investigated how a special antibody, UMCD6, affects immune cells that fight cancer. Researchers found that UMCD6 helps these immune cells, particularly natural killer (NK) cells and certain T cells, become more effective at killing cancer cells in mice with breast and prostate cancer, leading to improved survival rates. Specifically, treated mice had more powerful immune cells that were better positioned to attack tumors compared to those treated with a standard antibody.
Who this helps: This benefits cancer patients by potentially improving treatments that enhance their immune responses to tumors.
Activation of Cytotoxic Lymphocytes Through CD6 Enhances Killing of Cancer Cells.
2023
Research square
Gurrea-Rubio M, Wu Q, Amin MA, Tsou PS, Campbell PL +14 more
Plain English This study looked at a specific way to boost the immune system's ability to fight cancer by focusing on a molecule called CD6. Researchers found that using an antibody (UMCD6) to block the interaction between CD6 and a protein found on many cancer cells (CD318) led to better survival rates in mice with breast and prostate cancer. In these mice, more immune cells that attack tumors, like NK and CD8+ T cells, were present and more active compared to those that didn’t receive the treatment.
Who this helps: This benefits cancer patients by potentially improving treatment outcomes.
Inhibition of bromodomain extraterminal histone readers alleviates skin fibrosis in experimental models of scleroderma.
2022
JCI insight
Vichaikul S, Gurrea-Rubio M, Amin MA, Campbell PL, Wu Q +14 more
Plain English This study looked at how blocking certain proteins called bromodomain extraterminal (BET) proteins can help reduce skin thickening in a condition known as scleroderma. The researchers found that using a drug called JQ1 to inhibit these proteins led to a significant reduction in fibrosis in lab animals and skin cells from scleroderma patients. Specifically, they observed changes in gene activity that affect cell growth and calcium levels, which are important for managing tissue fibrosis.
Who this helps: This benefits patients with scleroderma by offering potential new treatment options.
Soluble CD13 induces inflammatory arthritis by activating the bradykinin receptor B1.
2022
The Journal of clinical investigation
Tsou PS, Lu C, Gurrea-Rubio M, Muraoka S, Campbell PL +26 more
Plain English Researchers discovered that a protein called CD13, which leaks into the bloodstream, causes inflammatory arthritis by activating a receptor called B1R found on joint cells. They confirmed this by showing that blocking B1R with drugs stopped the inflammation in multiple types of arthritis in mice and in human joint tissue samples.
This matters because B1R could be a new drug target to treat rheumatoid arthritis and other inflammatory diseases by preventing CD13 from triggering joint inflammation.