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• W2080003147 abstract "Blood basophils are reduced in chronic urticaria and respond less well to immunologic stimuli. Active recruitment of basophils from peripheral blood into lesional skin may be important in wheal pathogenesis. Blood basophils are reduced in chronic urticaria and respond less well to immunologic stimuli. Active recruitment of basophils from peripheral blood into lesional skin may be important in wheal pathogenesis. Not much is known about the physiology and fate of basophils in urticaria, but it is possible that they have a direct role because “releasability” to anti-IgE has been shown to be reduced and peripheral blood basopenia appears to relate to serum histamine releasing activity in chronic disease. Preliminary findings indicate that numbers are negatively correlated with urticarial activity, supporting the hypothesis that they migrate from blood into skin during wheal formation and contribute to persistence of the wheal. Basophils comprise about 1% of the circulating granulocytes in humans. In healthy subjects this represents about 40 basophils per µl of whole blood, which equates to around 200 million in the circulation at any time. They are characterized by granules that stain with basic dyes. Despite many similarities with tissue mast cells they show developmental, phenotypic, and functional differences. Basophils and mast cells almost certainly arise from a common bone marrow stem cell. Whereas the conditions required for maturation of the basophil are unclear, the phenotype of tissue mast cells is controlled by the local cytokine environment. Mucosal mast cells containing tryptase (MCT cells) mature under the influence of interleukins 3 and 4, but connective tissue mast cells containing tryptase and chymase (MCTC) require the presence of fibroblasts. The survival of blood basophils is unknown but is probably less than mast cells. The fate of basophils that have degranulated in response to a stimulus is not certain, but recovery of the granules within 6 h appears possible (Dvorak et al., 1996Dvorak A.M. Warner J.A. Fox P. Lichtenstein L.M. MacGlashan D.W. Recovery of human basophils after FMLP-stimulated secretion.Clin Exp Allergy. 1996; 26: 281-294Crossref PubMed Scopus (12) Google Scholar) and basophils are capable of division (Stock and Hoffman, 2000Stock W. Hoffman R. White blood cells 1: non-malignant disorders.Lancet. 2000; 355 (10.1016/s0140-6736(00)02125-5): 1351-1357Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar). Both basophils and mast cells express the high-affinity IgE receptor (FcαRI) and release preformed histamine, which is the major mediator of urticaria. Secondary mediators, newly synthesized on degranulation, differ in their proportions: leukotriene C4 is formed by basophils whereas mast cells predominantly form prostaglandin D2. Stimulated mast cells produce a wide range of cytokines, including IL-1, -3–8, -10, -13, GM-CSF, IFN-γ, and TNF-α, but cytokine expression by activated basophils is restricted to IL-4 and -13. There is relatively little literature on basophils in health and disease. This is partly because they are present in low numbers in peripheral blood and are difficult to quantify accurately with automated differentials. Basophils and mast cells cannot be distinguished easily in tissue with conventional stains. Most of the current literature relates to the use of basophils in the diagnosis of allergic disease and histamine releasing activity of serum in urticaria, using assays of functional activity. Basophil releasability (as defined by maximum histamine release with a defined stimulus) was shown to be reduced with anti-IgE in chronic urticaria basophils byGreaves et al., 1974Greaves M.W. Plummer V.M. McLaughlan P. Stanworth D.R. Serum and cell bound IgE in chronic urticaria.Clin Allergy. 1974; 4: 265-271Crossref PubMed Scopus (65) Google Scholar and Lichtenstein (Kern and Lichtenstein, 1976Kern F. Lichtenstein L.M. Defective histamine release in chronic urticaria.J Clin Invest. 1976; 57: 1369-1377Crossref PubMed Scopus (116) Google Scholar) in the 1970s, although the explanation for this was not clear at the time. The much later finding of functional anti-IgE (Grattan et al., 1991Grattan C.E.H. Francis D.M. Hide M. Greaves M.W. Detection of circulating histamine releasing autoantibodies with functional properties of anti-IgE in chronic urticaria.Clin Exp Allergy. 1991; 21: 695-704Crossref PubMed Scopus (294) Google Scholar) and anti-FcαRI (Hide et al., 1993Hide M. Francis D.M. Grattan C.E.H. Hakimi J. Kochan J.P. Greaves M.W. Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria.New Engl J Med. 1993; 328: 1599-1604Crossref PubMed Scopus (767) Google Scholar) autoantibodies in the serum of some chronic “idiopathic” urticaria patients implies that circulating basophils in these patients may be in a state of desensitization from further stimulation through the FcαRI.Zuberbier et al., 1996Zuberbier T. Schwarz S. Hartmann K. Pfrommer C. Czarnetski B.M. Histamine releasability of basophils and skin mast cells in chronic urticaria.Allergy. 1996; 51: 24-28Crossref PubMed Scopus (22) Google Scholar confirmed the reduction of basophil releasability in chronic urticaria with anti-IgE as the stimulus, but found this did not apply to skin mast cells.Sabroe et al., 1998Sabroe R.A. Francis D.M. Barr R.M. Kobza Black A. Greaves M.W. Anti-FcαRI autoantibodies and basophil histamine releasability in chronic idiopathic urticaria.J Allergy Clin Immunol. 1998; 102: 651-658Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar demonstrated reduced basophil releasability in chronic urticaria with anti-IgE and a murine monoclonal antibody against the FcαRI but not FMLP. The greatest reduction was seen with autoantibody-positive patients. Blood basophils may be increased in myxedema and diabetes mellitus and reduced in hyperthyroidism, pregnancy, ovulation, after administration of corticosteroids, and in chronic urticaria (Sabroe et al., 1998Sabroe R.A. Francis D.M. Barr R.M. Kobza Black A. Greaves M.W. Anti-FcαRI autoantibodies and basophil histamine releasability in chronic idiopathic urticaria.J Allergy Clin Immunol. 1998; 102: 651-658Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar;Rorsman, 1961Rorsman H. Basopenia in urticaria.Acta Allergologica. 1961; 16: 185-215Crossref PubMed Scopus (13) Google Scholar;Rorsman et al., 1962Rorsman H. Slatkin M.W. Harber L.C. Baer R.L. The basophil leukocyte in urticarial hypersensitivity to physical agents.J Invest Dermatol. 1962; 39: 493-499Abstract Full Text PDF PubMed Scopus (3) Google Scholar;Grattan et al., 1997Grattan C.E.H. Walpole D. Francis D.M. et al.Flow cytometric analysis of basophil numbers in chronic urticaria: basopenia is related to serum histamine releasing activity.Clin Exp Allergy. 1997; 27: 1417-1424Crossref PubMed Scopus (83) Google Scholar). Urticaria appears to be the only clinical disorder where basophil enumeration may be of immediate clinical relevance.Rorsman, 1961Rorsman H. Basopenia in urticaria.Acta Allergologica. 1961; 16: 185-215Crossref PubMed Scopus (13) Google Scholar found that peripheral blood basophils were reduced in idiopathic urticaria (mean 5 per µl) by comparison with healthy subjects (45 per µl) using a metachromatic granule stain on peripheral blood, but were not reduced in physical urticarias (Rorsman et al., 1962Rorsman H. Slatkin M.W. Harber L.C. Baer R.L. The basophil leukocyte in urticarial hypersensitivity to physical agents.J Invest Dermatol. 1962; 39: 493-499Abstract Full Text PDF PubMed Scopus (3) Google Scholar). He also noted that the basopenia of urticaria was only sustained during periods of disease activity. His results were later confirmed and extended byGrattan et al., 1997Grattan C.E.H. Walpole D. Francis D.M. et al.Flow cytometric analysis of basophil numbers in chronic urticaria: basopenia is related to serum histamine releasing activity.Clin Exp Allergy. 1997; 27: 1417-1424Crossref PubMed Scopus (83) Google Scholar who found that blood basophil numbers in chronic “idiopathic” urticaria related to the histamine releasing activity of serum from the same patients. Those with serum activity that released histamine from basophils of healthy donors had few or absent circulating basophils. This was true whether the counts were done with a manual counting chamber method using toluidine blue staining of basophil granules or flow cytometry employing a dual stain for membrane markers, indicating that the cells had disappeared from the circulation rather than being rendered invisible to granule stains by activation.Sabroe et al., 1998Sabroe R.A. Francis D.M. Barr R.M. Kobza Black A. Greaves M.W. Anti-FcαRI autoantibodies and basophil histamine releasability in chronic idiopathic urticaria.J Allergy Clin Immunol. 1998; 102: 651-658Abstract Full Text Full Text PDF PubMed Scopus (93) Google Scholar looked at chronic urticaria patients with or without evidence of functional autoantibodies (defined by histamine releasing activity) and found that the mean numbers were reduced in nonantibody patients (although less so than anitbody-positive patients) when compared with controls. There were comparable reductions in total cellular blood histamine in each group. The fate of the missing blood basophils in chronic urticaria remains unclear. It is possible that they are actively recruited into wheals by expression of endothelial adhesion molecules, including VCAM-1, induced by degranulation of lesional skin mast cells. This might explain the prolongation of “idiopathic” urticaria wheals well beyond the expected time course of histamine-induced wheals in healthy subjects (Cook and Shuster, 1980Cook J. Shuster S. Histamine weal formation and absorption in man.Br J Pharmacol. 1980; 69: 579-585Crossref PubMed Scopus (56) Google Scholar). A 14-fold increase of basophil numbers was found in biopsies of the late cutaneous response of immediate hypersensitivity reactions to antigen challenge, which correlated with a late increase in tissue histamine (Charlesworth et al., 1989Charlesworth E.N. Hood A.F. Soter N.A. et al.Cutaneous late-phase response to allergen. Mediator release and inflammatory cell infiltration.J Clin Invest. 1989; 83: 1519-1526Crossref PubMed Scopus (222) Google Scholar). Binding of FcαRI on cutaneous mast cells by autoantibodies rather than allergen could have similar consequences in chronic urticaria. Histologic studies of urticarial wheals using monoclonal antibody stains for basophil membrane markers should address this. Recent work has been focused on measuring blood basophil numbers in relation to urticarial activity over the course of a day and assessing the effects of treatment with antihistamines and oral corticosteroids. It might be expected that a reduction in urticarial wheals would lead to an increase in blood basophils if active recruitment into lesional skin is inhibited. Preliminary analysis of the study results shows that there is little variation in blood basophil numbers over the day in healthy controls and chronic urticaria patients off treatment, although a marked basopenia was present in the urticaria patients. A sharp reduction of basophil numbers was seen in healthy controls after taking oral corticosteroids from around 45 per µl to10 per µl of whole blood. Conversely, basophil numbers increased from around 5 per µl to 10 per µl in the chronic urticaria patients. These results suggest there is a two-way traffic of circulating basophils between blood and tissues in health and disease. As well as inhibiting IL-4 secretion (Schroeder et al., 1997Schroeder J.T. MacGlashan D.W. MacDonald S.M. Kagey-Sobotka A. Lichtenstein L.M. Regulation of IgE-dependent IL-4 generation by human basophils treated with glucocorticoids.J Immunol. 1997; 158: 5448-5454PubMed Google Scholar) and IgE-dependent histamine release (Schleimer et al., 1982Schleimer R.P. MacGlashan D.W. Gillespie E. Lichtenstein L.M. Inhibition of basophil histamine release by anti-inflammatory steroids. II. Studies on the mechanism of action.J Immunol. 1982; 129: 1632-1636PubMed Google Scholar) from basophils, it seems that corticosteroids may influence endothelial mechanisms (such as constitutive adhesion molecule expression) that regulate the return of migrating basophils to the circulation when not actively engaged in tissue inflammation. A significant negative linear correlation between blood basophil numbers and urticarial activity scores lends some support to the hypothesis that they may contribute directly to the pathogenesis of urticarial wheals in “idiopathic” urticaria." @default.
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• W2080003147 title "Basophils in Chronic Urticaria" @default.
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