Scleroderma Program, Division of Rheumatology, Department of Internal Medic, University of Michigan Medical School, Ann Arbor, United States of America.
Sirapa Vichaikul studies the mechanisms behind inflammatory arthritis, particularly rheumatoid arthritis. She investigates how certain proteins like CD13 can leak into the bloodstream and trigger inflammation by activating specific receptors on immune cells. By understanding this activation, she aims to find new ways to treat rheumatoid arthritis by blocking these receptors without suppressing the entire immune system, which can have widespread effects.
Key findings
Blocking the bradykinin receptor B1 (B1R) significantly reduces inflammation in human tissue samples and mouse models of arthritis.
The B1R receptor is overactive in patients with rheumatoid arthritis, contributing to the disease's severity.
Identifying CD13 as a key player in inflammatory arthritis opens a pathway to new treatments that target the B1R receptor specifically.
Frequently asked questions
Does Dr. Vichaikul study rheumatoid arthritis?
Yes, Dr. Vichaikul focuses on rheumatoid arthritis and the mechanisms that cause inflammation in this condition.
What treatments has Dr. Vichaikul researched?
She has researched treatments that target the bradykinin receptor B1 to reduce inflammation without broadly affecting the immune system.
Is Dr. Vichaikul's work relevant to people with inflammatory diseases?
Yes, her research on CD13 and B1R could lead to new treatment options for inflammatory diseases beyond just rheumatoid arthritis.
Publications in plain English
A potent inhibitor of PAI-1, MDI-2517, mitigates disease severity in a preclinical systemic sclerosis model.
2026
JCI insight
Su EJ, Tsou PS, Warnock M, Subbotina N, Mann K +14 more
Plain English This study looked at systemic sclerosis (SSc), a disease that causes thickening and scarring of the skin and other organs. Researchers found that a substance called PAI-1 is linked to the disease, and when they treated mice with a new drug called MDI-2517, it significantly reduced scarring in the skin and lungs, outperforming existing treatments. Specifically, MDI-2517 worked better at a much lower dose compared to another treatment, showing promise as a new way to help patients with SSc.
Who this helps: Patients with systemic sclerosis.
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.
Functional Characterization of Glycoprotein Nonmetastatic Melanoma Protein B in Scleroderma Fibrosis.
2022
Frontiers in immunology
Palisoc PJ, Vaikutis L, Gurrea-Rubio M, Model EN, O'mara MM +5 more
Plain English This study looked at how a protein called GPNMB behaves in the skin cells of patients with diffuse cutaneous scleroderma (dcSSc), a condition that causes skin thickening. Researchers found that the levels of GPNMB were higher in skin cells from dcSSc patients compared to healthy individuals, with notable levels of its soluble form measured at 147.4 pg/ml versus 84.8 pg/ml. This protein appears to help reduce cell activity that leads to fibrosis, suggesting that boosting GPNMB could be a new way to treat scleroderma.
Who this helps: This benefits patients with scleroderma.
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.