Human basophils and mast cells express the chemokine receptor CCR3, which binds the chemokines eotaxin and RANTES. HIV-1 Tat protein is a potent chemoattractant for basophils and lung mast cells obtained from healthy individuals seronegative for Abs to HIV-1 and HIV-2. Tat protein induced a rapid and transient Ca2+ influx in basophils and mast cells, analogous to β-chemokines. Tat protein neither induced histamine release from human basophils and mast cells nor increased IL-3-stimulated histamine secretion from basophils. The chemotactic activity of Tat protein was blocked by preincubation of FcεRI+ cells with anti-CCR3 Ab. Preincubation of Tat with a mAb anti-Tat (aa 1–86) blocked the migration induced by Tat. In contrast, a mAb specific for the basic region (aa 46–60) did not inhibit the chemotactic effect of Tat protein. Tat protein or eotaxin desensitized basophils to a subsequent challenge with the autologous or the heterologous stimulus. Preincubation of basophils with Tat protein up-regulated the level of CCR3 mRNA and the surface expression of the CCR3 receptor. Tat protein is the first identified HIV-1-encoded β-chemokine homologue that influences the directional migration of human FcεRI+ cells and the expression of surface receptor CCR3 on these cells.

Background: The aim of this study was to investigate whether human mast cells express functional active CCR3 receptors, which are activated by CC chemokines. These ligands include the CCR3-selective chemokines eotaxin and eotaxin-2 and the more promiscuous CC chemokines, MCP-4, MCP-3, MCP-2 and RANTES. Methods: Immunohistochemical analysis was performed on skin, gut and lung specimens. Double immunostaining was performed with anti-CCR3 and antitryptase, and anti-CCR3 and antichymase antibody (Ab) by using the avidin-biotin-peroxidase system with two different substrates. Mast cells were isolated and purified from human lung parenchyma (HLMC) by countercurrent elutriation followed by discontinuous Percoll density gradient. Flow-cytometric analysis of HLMC surface CCR3 expression was performed with the monoclonal Ab anti-CCR3 (7B11). Functional activation of HLMC was verified by the ability of cells to release histamine and/or migrate in response to eotaxin. Results: High percentages (>70%) of tryptase-positive cells showing CCR3 expression were found in the skin and in the intestinal submucosa, whereas much lower percentages (≤20%) were found in the intestinal mucosa and in the lung interstitium. Eotaxin (1–100 nM) neither induced histamine release from HLMC nor enhanced anti-IgE-induced histamine release. In contrast, eotaxin (10–100 nM) and RANTES (10–100 nM) induced HLMC chemotaxis in vitro. Preincubation of HLMC with antibody anti-CCR3 (5 µg/ml) before loading into the chemotaxis chamber abrogated chemotaxis elicited by eotaxin. Double immunostaining with anti-CCR3 and anti-chymase antibody showed that the vast majority of CCR3-expressing mast cells in the various human tissues examined were tryptase-chymase double-positive. Conclusions: These results indicate that CCR3 is expressed on human mast cells and that these cells are attracted by CCR3-binding chemokines.

Ankle impingement is defined as entrapment of an anatomic structure that leads to pain and decreased range of motion of the ankle and can be classified as either soft tissue or osseous (Bassett et al. in J Bone Joint Surg Am 72:55-59, 1990). The impingement syndromes of the ankle are a group of painful disorders that limit full range of movement. Symptoms are due to compression of soft-tissues or osseous structures during particular movements (Ogilvie-Harris et al. in Arthroscopy 13:564-574, 1997). Osseous impingement can result from spur formation along the anterior margin of the distal tibia and talus or as a result of a prominent posterolateral talar process, the os trigonum. Soft-tissue impingement usually results from scarring and fibrosis associated with synovial, capsular, or ligamentous injury. Soft-tissue impingement most often occurs in the anterolateral gutter, the medial ankle, or in the region of the syndesmosis (Van den Bekerom and Raven in Knee Surg Sports Traumatol Arthrosc 15:465-471, 2007). The main impingement syndromes are anterolateral, anterior, anteromedial, posterior, and posteromedial impingement. These conditions arise from initial ankle injuries, which, in the subacute or chronic situation, lead to development of abnormal osseous and soft-tissue thickening within the ankle joint. The relative contributions of the osseous and soft-tissue abnormalities are variable, but whatever component is dominant there is physical impingement and painful limitation of ankle movement. Conventional radiography is usually the first imaging technique performer and allows assessment of any potential bone abnormality, particularly in anterior and posterior impingement. Computed tomography (CT) and isotope bone scanning have been largely superseded by magnetic resonance (MR) imaging. MR imaging can demonstrate osseous and soft-tissue edema in anterior or posterior impingement. MR imaging is the most useful imaging modality in evaluating suspected soft-tissue impingement or in excluding other ankle pathology such as an osteochondral lesion of the talus. MR imaging can reveal evidence of previous ligamentous injury and also can demonstrate thickened synovium, fibrosis, or adjacent reactive soft-tissue edema. Studies of conventional MR imaging have produced conflicting sensitivities and specificities in assessment of anterolateral impingement. CT and MR arthrographic techniques allow the most accurate assessment of the capsular recesses, albeit with important limitations in diagnosis of clinical impingement syndromes. In the majority of cases, ankle impingement is treated with conservative measures, with surgical debridement via arthroscopy or an open procedure reserved for patients who have refractory symptoms. In this article, we describe the clinical and potential imaging features, for the four main impingement syndromes of the ankle: anterolateral, anterior, anteromedial, posterior, and posteromedial impingement.

Ultrasound has a good diagnostic accuracy in identifying the chondral print sign.