**1. Introduction**

Cell membrane microparticles (MPs), or microvesicles, are fragments of surface membranes of activated eukaryotic cells. Their size, which determines their diameter as lying within the interval of 0.1 to 1 μm, is their main defining criterion. Therefore, the diameter of MPs is greater than that of exosomes and smaller than that of apoptotic bodies or small platelets. In physiological conditions, when cells mature, age, and undergo apoptosis, microparticles are released by exfoliation or by shedding to body fluids from cell membranes of all morphotic elements of blood and vascular endothelium [1,2]. MPs can be found in plasma, in whole blood, in umbilical blood, in cerebrospinal fluid, in urine, in

milk, and in saliva. Microparticles do not have a cell nucleus, but they contain cytoplasmic material and surface antigens of their parent cells, owing to which their origin can be determined [2–4] (Table 1). Increased secretion of MPs in physiological conditions takes place in pregnant women, after intensive physical effort, in obese people, and in smokers [5]. Increased secretion of microparticles from activated platelets, leukocytes, erythrocytes, smooth muscle cells, and vascular endothelium cells takes place in immune-mediated diseases. An increased number of microparticles have been found in immune thrombocytopenia [6], in systemic lupus erythematosus [7], in rheumatoid arthritis [8], and in psoriasis [9,10]. The presence in MPs membrane of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) enables microparticles to join other cells and to take part in intermembrane transport of enzymes and receptor proteins, cytokines, growth factors, and nucleic acids: Micro RNA (miRNA), messenger RNA (mRNA), and deoxyribonucleic acid (DNA) [11,12].


**Table 1.** Cells of origin of microparticles and their clusters of differentiation.

CD—cluster of differentiation, MPs—microparticles, PS—phosphatidylserine, TF—tissue factor.

As many as 90% of all circulating microparticles areMPs derived from platelets and megakaryocytes (PMPs) [13]. PMPs have a number of receptors on their membrane surface, including adhesive proteins. For PMPs, the most frequent surface markers are: Glycoprotein IIb (CD41), Ib (CD42b), IIb/IIIa (CD41a), IIIa (CD61), selectin P (CD62P) [3], and sphingolysine, arachidonic acid (AA), and bioactive lipids [5,14,15]. Contact of platelet-derived microparticles with target cells can result in monocyte chemotaxis, stimulation of cytokine secretion, activation of endothelial cells, and increased tissue factor expression on endothelial cell surface [16]. Platelet microparticles stimulate phagocytic activity of granulocytes by increasing the expression of the adhesive molecule CD11b on them [17]. An increased number of platelet-derived microparticles have been observed in atherosclerosis [18], diabetes [19], coronary artery disease [20], thrombotic thrombocytopenic purpura [21], aplastic anaemia, and paroxysmal nocturnal haemoglobinuria [22]. However, it is very likely that the activation of monocytes/macrophages, B-cells, T-cells, and endothelial cells observed in patients with inflammatory diseases may result in an increased release of MPs from these cells, raising their levels in plasma.

It has been proposed that excessive production of MPs may predispose to autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus [23] but their role in the pathogenesis of these autoimmune diseases may differ. In patients with SLE, a prototypic autoimmune disease characterized by the production of antibodies to components of the cell nucleus and the formation of immune complexes, circulating MPs differ in their amount and composition compared to from those in patients with RA or healthy controls. MPs from SLE patients contain more immunoglobulins (IgG, IgA, and IgM) and complement components (C1q, C1s, C3, C4b, and C9) on their surface indicating the role of MPs as a source of immune complexes [24]. MPs containing DNA and RNA in SLE can behave as self-adjuvants for the production of autoantibodies. They can also increase tolerance of immature B-lymphocytes and break the tolerance of mature B-cells. MPs endocytosed by plasmacytoid dendritic cells are able to contact intracellular TLR7 (toll-like receptor-7) and TLR9, leading to the production of proinflammatory cytokines including type 1 interferon (IFN-1) and IL-6 (interleukin-6) [25].
