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Hemophagocytic lymphohistiocytosis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Aradhana Sood, Deep Kumar Raman, Pankaj Das
Bone marrow studies are mandatory in suspected HLH cases to detect hemophagocytosis and to rule out other causes of cytopenias and malignancies. The cellularity of the marrow is variable, and hemophagocytosis is seen in 25%–100% of HLH but may not be evident in the initial stage of the disease [20]. Macrophages can be highlighted by CD163 staining.
Immunology of Skin and Reactivity
Published in Heather A.E. Benson, Michael S. Roberts, Vânia Rodrigues Leite-Silva, Kenneth A. Walters, Cosmetic Formulation, 2019
Krishna Telaprolu, Heather A.E. Benson, Jeffrey E. Grice, Michael S. Roberts, Philip L. Tong
The various macrophages present in the skin are M1 proinflammatory macrophages that are activated by IFN-γ or by microbial products, and contribute to both acute and chronic inflammation in the skin. Proinflammatory macrophages expressing CD163 are found in psoriasis, atopic dermatitis and cutaneous T cell lymphoma (Sugaya et al., 2012). M2 wound-healing macrophages are known to regulate the skin inflammatory response through IL-10 and transforming growth factor-β (TGFβ). M2 macrophages are induced by IL-4 and -13 and promote type 2 immune responses by capturing antigens and reducing their availability to lymphocytes. The skin resident macrophages along with the circulating monocytes support the DCs in immunosurveillance and in the transport of antigens to the draining lymph nodes (Fuentes-Duculan et al., 2010).
HIV and Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
There is increasing evidence for the role of immune dysfunction of monocytes during HIV infection [55]. Chronic immune activation of monocytes can be indicated by the biomarkers IL-6, soluble CD14, and soluble CD163 in serum. Activation is believed to be caused by increased microbial translocation, residual HIV replication, and reactivation of other viruses including CMV. Monocyte activation has been associated with cardiovascular disease and HIV-associated neurocognitive disorder.
Circulating biomarkers of response to immunotherapy and immune-related adverse events
Published in Expert Review of Molecular Diagnostics, 2022
Zachary Garrison, Noah Hornick, Jeffrey Cheng, Rajan P. Kulkarni
CXCL5 is a member of a family of angiogenic chemokines that include CXCL1, CXCL2, CXCL3, CXCL6, CXCL7, and CXCL8. It has long been studied for its role in inflammation and cancer development [80]. More recently, CXCL5 has been identified as a biomarker of TH-17 cell-mediated autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and pemphigus vulgaris [81–83]. This influence on inflammation has also been observed to extend to immune therapy-induced irAEs. A study of advanced melanoma patients on nivolumab identified changes to CXCL5 levels for several types of inflammatory related irAEs including hypophisitis, thyroid dysfunction, adrenal insufficiency, psoriasiform dermatitis, interstitial pneumonia, hepatitis, radiation dermatitis, rheumarthritis, biliary tract disorder, and bursitis, though they did not find a significant trend in their limited sample size [84]. This relationship was also correlated with serum levels of CD163 expressing macrophages. CD163, a receptor found on monocytes [85,86], is linked to CXCL5 via their shared presence on tumor associated macrophages (TAMs). TAM production of CXCL5 [87] is the most rational explanation for the parallel correlation of CXCL5/CD163 and irAEs. CD163+ macrophages are a key component of tumor infiltrating immune cells that produce chemokines associated with cancer development and inflammation [88]. They have already been identified as a marker of autoimmune diseases such as rheumatoid arthritis, pemphigus vulgaris, and bullous pemphigoid [85].
Soluble CD163 is a potential biomarker in systemic sclerosis
Published in Expert Review of Molecular Diagnostics, 2019
Takashi Matsushita, Kazuhiko Takehara
M2 macrophages express CD163 as a scavenger receptor involved in the removal of necrotic cells, apoptotic cells, cell debris, and opsonized pathogens. Therefore, CD163 is thought to represent an M2 macrophage marker. The primary function of CD163 is uptake of circulating haptoglobin–hemoglobin complexes from circulating blood [5]. Additionally, CD163 is a receptor for ADAMTS13 and tumor necrosis factor-like weak inducer of apoptosis (TWEAK). Soluble CD163 (sCD163) is released from the cell surface of M2 macrophages by proteolysis in response to oxidative stress or inflammatory stimuli and exerts anti-inflammatory effects by inhibiting T cell proliferation [6]. In SSc patients, levels of CD14+ monocytes in the blood are significantly increased relative to those observed in healthy controls, and CD14+ monocytes in SSc patients display elevated expression of CD163 [7]. Moreover, number of CD163+ M2 macrophages in the skin of SSc patients are significantly elevated relative to those in healthy controls [7]. Furthermore, circulating monocytes in SSc patients having ILD exhibit increased CD163 expression in response to LPS stimulation as compared with those in normal controls [8], with another study reporting elevated CD163 mRNA levels in SSc patients with ILD relative to those in healthy controls, being positively associated with ILD severity [9]. These findings represent emerging evidence that M2 macrophages play a distinctive role in SSc pathogenesis.
Renal involvement in paroxysmal nocturnal hemoglobinuria: an update on clinical features, pathophysiology and treatment
Published in Hematology, 2018
Styliani I Kokoris, Eleni Gavriilaki, Aggeliki Miari, Αnthi Travlou, Elias Kyriakou, Achilles Anagnostopoulos, Elissavet Grouzi
In classical PNH, red cell intravascular hemolysis is continuous and appears in various degrees. When hemoglobin is free in the plasma, it exists mostly as alpha/beta dimers that rapidly complex to haptoglobin (Hp), a liver-produced plasma protein. This is the first mechanism of hemoglobin iron salvage. By binding to Hp, hemoglobin avoids filtration at the glomerulus and the release of its heme moiety is prevented [33]. More specifically, the haptoglobin–hemoglobin complexes are too large to be filtered by the glomerulus, so they are carried to the liver, where they are recognized by the CD163 receptors (these are membrane proteins expressed on monocyte/macrophage surfaces and hepatocytes) [34–36]. The binding of the hemoglobin molecules to CD163 receptors results in the neutralization of free hemoglobin’s toxic actions. Hemoglobin, also, has the ability to up-regulate CD163’s expression. The uptake of hemoglobin by CD163 receptors not only attenuates the toxic effects of cell-free hemoglobin, but it also induces several anti-inflammatory responses, including interleukin-10 release and heme oxygenase-1 synthesis (HO-1) [15]. In cases where hemolysis is accelerated, Hp molecules are depleted, due to the liver’s inability to increase Hp’s production as a response to the increased hemolysis: Hp molecules are typically adequate to salvage only a normal amount of plasma hemoglobin.