Immunohistochemical detection of human basophils in late-phase skin reactions

Urokinase Induces Basophil Chemotaxis through a Urokinase Receptor Epitope That Is an Endogenous Ligand for Formyl Peptide Receptor-Like 1 and -Like 2

“…Our results are compatible with the hypothesis that uPA-dependent chemotaxis is mediated by the exposure of a chemotactic urokinase receptor epitope that is an endogenous agonist for FPRL2 on human basophils. Finally, the results described in this study may have practical implications in disorders such as allergic diseases and certain bacterial infections in which basophils infiltrating the sites of inflammation play a prominent role (57,(65)(66)(67). In fact, it is conceivable that agents acting on uPAR-mediated chemotaxis (i.e., by blocking the chemotactic epitope) may be used to modify the basophildriven inflammatory reactions.…”

CCR3-Blocking Antibody Inhibits Allergen-Induced Eosinophil Recruitment in Human Skin Xenografts from Allergic Patients

“…This recruitment is orchestrated in part by chemokines that act through specialized surface receptors. The chemokine receptor CCR3 is of particular interest in the context of allergic reactions, because it is expressed by TH2 lymphocytes (Sallusto et al, 1997), eosinophils (Ponath et al, 1996), basophils (Uguccioni et al, 1997), and mast cells (Ochi et al, 1999;Romagnani et al, 1999), all of which are found at sites of allergen-induced latephase response (LPR) (Frew and Kay, 1988;Gaga et al, 1991;Irani et al, 1998). The CCR3 receptor is a Gprotein-coupled seven-transmembrane receptor that mediates the action of several chemokines, including eotaxin (CCL11), RANTES (CCL5), MCP-3 (CCL7), and MCP-4 (CCL13) (Ponath et al, 1996;Stellato et al, 1997).…”

“…In humans, allergen-induced cutaneous LPR is associated with an infiltration of CD4 ϩ T cells, eosinophils, activated CD25 ϩ cells (Barata et al, 1998;Tsicopoulos et al, 1994), and basophils (Irani et al, 1998;Ying et al, 1999). A preferential TH2-type cytokine mRNA expression with almost no TH1 expression is found at the sites of such cutaneous allergic reactions Tsicopoulos et al, 1994).…”

“…No human cell migration was observed when allergen was injected into mouse skin in the reconstituted SCID mouse model, and without PBMC, no LPR occurred in allergen-injected human allergic skin of grafted SCID mice. Taken together, the allergen challenge of skin xenografts from allergic donors in reconstituted SCID mice resulted in the development of an immediate reaction and a delayed reaction exactly as observed in skin from allergic patients.In humans, allergen-induced cutaneous LPR is associated with an infiltration of CD4 ϩ T cells, eosinophils, activated CD25 ϩ cells (Barata et al, 1998;Tsicopoulos et al, 1994), and basophils (Irani et al, 1998;Ying et al, 1999). A preferential TH2-type cytokine mRNA expression with almost no TH1 expression is found at the sites of such cutaneous allergic reactions Tsicopoulos et al, 1994).…”

Transendothelial Migration of Human Basophils

“…The results of experimental allergen challenge in various organs have revealed the influx of basophils to inflammatory sites several hours after Ag exposure (5)(6)(7)(8)(9), indicating the existence of a mechanism for recruitment of basophils from the blood compartment to inflamed tissue sites during allergic reactions. Like other types of leukocytes, the entire process of basophil influx to inflamed tissue sites comprises three essential sequential steps: adhesion to the vascular endothelium, transendothelial migration (TEM), 3 and locomotion toward inflammatory sites in extravascular tissues.…”