CD106 is a protein known more commonly as Vascular Cell Adhesion Molecule-1, or VCAM-1. As a cell adhesion molecule, it functions like a specialized patch on cell surfaces. CD106 helps cells stick to each other or to the surrounding environment. Its presence plays a role in the immune system’s ability to respond to challenges and in how blood vessels interact with various cell types.
The Function of CD106
CD106 acts like one half of a lock-and-key mechanism on the surface of certain cells. Its primary function involves catching and binding to specific immune cells, known as leukocytes, as they flow through the bloodstream. These leukocytes include types such as lymphocytes and monocytes, which patrol the body.
The binding occurs when CD106 on the surface of blood vessel lining cells attaches to a complementary molecule on these immune cells. This complementary molecule is called integrin α4β1, also known as VLA-4. This interaction allows immune cells to slow down, roll along the vessel wall, and eventually adhere firmly. This process is a normal part of immune surveillance, enabling immune cells to exit the bloodstream and enter tissues where they can monitor for infections or perform maintenance.
Expression and Regulation
CD106 is not always present on cell surfaces; its production and display are carefully controlled. Its appearance, or “upregulation,” occurs in response to particular signals within the body. The primary triggers for CD106 production are pro-inflammatory cytokines, which are signaling proteins released by cells.
Two prominent cytokines that induce CD106 expression are tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1). When tissues experience damage, infection, or inflammation, nearby cells release these cytokines into the local environment. These cytokines then signal the endothelial cells, which form the inner lining of blood vessels, to begin producing and displaying CD106. This induced expression of CD106 acts as a specific beacon, guiding immune cells to sites of inflammation or injury.
Role in Inflammatory Diseases
When the regulation of inflammation is disrupted, the normal function of CD106 can contribute to the development and progression of chronic diseases. For example, in atherosclerosis, a condition where plaque builds up inside arteries, CD106 plays a part in the disease process. It appears on the inner lining of arterial walls and captures monocytes from the bloodstream. These monocytes then cross into the artery wall, where they absorb lipids and transform into foam cells, major components of atherosclerotic plaques.
In multiple sclerosis (MS), a disease affecting the brain and spinal cord, CD106 facilitates the entry of harmful immune cells into the central nervous system. CD106 expressed on the cells forming the blood-brain barrier helps destructive lymphocytes bind and cross this protective barrier. Once inside the brain and spinal cord, these lymphocytes launch attacks on the myelin sheath, the protective covering around nerve fibers, leading to neurological damage.
CD106 also contributes to the pathology of rheumatoid arthritis, an autoimmune disease causing chronic joint inflammation. It allows inflammatory cells to enter the joint spaces, where they release destructive enzymes and cytokines. This sustained influx of immune cells through CD106 interactions perpetuates the inflammation, leading to the erosion of cartilage and bone within the joints.
Clinical Significance and Therapeutic Targeting
The presence of CD106 has practical medical implications, including its potential as a biomarker. Elevated levels of soluble CD106, a version of the protein that circulates freely in the blood, can sometimes indicate the presence and severity of inflammatory conditions. Monitoring these levels can offer insights into disease activity or progression in certain inflammatory disorders.
Because CD106 is involved in the movement of immune cells to sites of inflammation, blocking its function represents a strategy for therapeutic intervention. Medications designed to interfere with the CD106 pathway can prevent the excessive accumulation of immune cells in inflamed tissues. An example of such a therapy is Natalizumab, a drug approved for treating multiple sclerosis and Crohn’s disease. Natalizumab works by specifically blocking integrin α4β1 (VLA-4) on immune cells, preventing it from binding to CD106 on blood vessel walls. This action restricts the ability of inflammatory cells to cross the blood-brain barrier and enter the central nervous system, reducing the autoimmune attack in MS patients.