Publications by authors named "Aleksandra Vuchkovska"

Article Synopsis
  • When skin gets hurt, special cells called hair follicle stem cells (HFSCs) move to help heal the wound but face tough inflammation.
  • These HFSCs activate certain proteins that help protect them and support healing, like CD80.
  • If HFSCs can’t use CD80, healing gets worse because they can’t call for help from other immune cells, which makes it harder for the skin to get better.
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Sialic acid-binding immunoglobulin-type lectins (Siglecs) are a family of immunoglobulin-type lectins that mediate protein-carbohydrate interactions via sialic acids attached to glycoproteins or glycolipids. Most of the CD33-related Siglecs (CD33rSiglecs), a major subfamily of rapidly evolving Siglecs, contain a cytoplasmic signaling domain consisting of the immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) and mediate suppressive signals for lymphoid and myeloid cells. While most CD33rSiglecs are expressed by innate immune cells, such as monocytes and neutrophils, to date, the expression of Siglecs in human T cells has not been well appreciated.

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Article Synopsis
  • - The fetal and neonatal immune systems are adapted to tolerate various antigens, which can help maintain a safe environment for the developing baby but may also leave them vulnerable to serious infections.
  • - A specific type of monocyte, known as CD14 CD36 monocytes, can generate T regulatory cells (Tregs) that help suppress immune responses and are essential for controlling inflammation and preventing graft-versus-host disease.
  • - Adult blood monocytes can also induce Tregs from both neonatal and adult stem cells; however, their capability is hindered by certain cells present in adult blood, revealing a complex relationship between different immune cells at varying life stages.
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Background: Alcohol consumption is a risk factor for impaired fracture healing, though the mechanism(s) by which this occurs are not well understood. Our laboratory has previously shown that episodic alcohol exposure of rodents negatively affects fracture callus development, callus biomechanics, and cellular signaling which regulates stem cell differentiation. Here, we examine whether alcohol alters chemokine expression and/or signaling activity in the mouse fracture callus during early fracture healing.

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Objectives: To explore how alcohol affects the BMP-2 signaling pathway, which is known to play a critical role in bone and cartilage formation during fracture healing.

Methods: A rat model was used to demonstrate the detrimental effects of alcohol exposure on tibia fracture healing. Specific components of the BMP-2 pathway were analyzed in fracture callus on days 3, 7, 14, and 21 after fracture via western immunoassays and enzyme-linked immunosorbent assay.

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The process of fracture healing is complex, and poor or incomplete healing remains a significant health problem. Proper fracture healing relies upon resident mesenchymal stem cell (MSC) differentiation into chondrocytes and osteoblasts, which are necessary for callus formation and ossification. Alcohol abuse is a leading contributor to poor fracture healing.

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