Researchers find that activated platelets secrete CCL5, which stimulates megakaryocytes to produce more platelets.
Blood platelets play an important role in many physiological conditions that occur in the body. Their main role is to limit bleeding and blood loss by forming clots at sites where the endothelial layer is disrupted. They are formed from fragments of the cytoplasm of megakaryocytic, large bone marrow progenitor cells that release proplatelets into the bloodstream. When conditions such as infections, inflammation or malignancy occur, there is a transient occurrence of a high platelet count. Their blood levels are important. A low platelet level lead to bleeding and too many can result in blood clots, so understanding how their numbers are regulated is important. However, it is still not clear how this occurs – well, until recently.
Researchers find that self-reactive IgE can worsen autoimmune inflammation in systemic lupus erythematosus patients.
Systemic lupus erythematosus (SLE), or as commonly known as lupus, is a chronic autoimmune disease that affects multiple organs in the body. In this disease, the immune system generates self-reactive immune cells and antibodies against the body’s nucleic acids. Lupus symptoms vary dramatically from one patient to another but usually include fever, pain, fatigue, abutterfly shaped rash on the cheeks and nose and skin lesions. Lupus can cause serious damage to major organs such as the kidneys, lungs and heart. Currently, there is no cure, only treatments to keep symptoms under control. Treatment usually includes non-steroidal anti-inflammatory drugs, corticosteroids or immunosuppressive therapy.1
Researchers find that Nr4a1 expression in macrophages link the sympathetic and immune systems and limit inflammation during multiple sclerosis.
It is becoming more apparent every day that the different systems of the human body influence each other substantially more than what was previously thought. New research provides evidence that this is the case with the immune and sympathetic nervous systems. The linking factor is macrophages and a transcription factor they express, Nr4a1, and the result is affecting the outcome of multiple sclerosis.