Các tế bào basophil và mast trong chứng mày đay tự phát mạn tính

Current Allergy and Asthma Reports - Tập 5 - Trang 270-276 - 2005
Becky M. Vonakis1, Sarbjit S. Saini1
1Department of Medicine, Division of Allergy and Clinical Immunology, The Johns Hopkins University School of Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, USA

Tóm tắt

Chứng mày đay tự phát mạn tính (CIU) được chẩn đoán ở bệnh nhân khi các tổn thương mày đay tái phát trong hơn 6 tuần và không xác định được nguyên nhân cụ thể. Với việc mày đay giống với các tổn thương do tiêm histamine hoặc tác nhân gây dị ứng vào da, một vai trò của tế bào mast hoặc basophil đã được đề xuất trong việc hình thành các tổn thương mày đay khu trú. Tuy nhiên, hiện tại, các cơ chế chính xác điều khiển sự kích hoạt tế bào mast hoặc basophil vùng là chưa rõ ràng. Trong thập kỷ qua, có sự quan tâm ngày càng tăng trong việc xem CIU như một bệnh tự miễn, do sự hiện diện của các tự kháng thể tuần hoàn đối với IgE hoặc tiểu đơn vị alpha của thụ thể IgE với độ ái lực cao (FcaRI) trong một nhóm nhỏ bệnh nhân. Trong bài tổng quan này, chúng tôi đề xuất rằng ngoài các tự kháng thể, sự khác biệt cụ thể trong biểu hiện của các phân tử tín hiệu FcaRI trong basophil hoặc tế bào mast của bệnh nhân CIU có thể góp phần vào sự hình thành các tổn thương mày đay.

Từ khóa

#Chứng mày đay tự phát mạn tính #tế bào mast #tế bào basophil #tự miễn #kháng thể tự động #thụ thể IgE

Tài liệu tham khảo

Kaplan AP: Chronic urticaria: pathogenesis and treatment. J Allergy Clin Immunol 2004, 114:465–474; quiz 75. Excellent review of current clinical treatments and autoantibody theory in CIU. Kaplan AP: Clinical practice: chronic urticaria and angioedema. N Engl J Med 2002, 346:175–179. Toubi E, Kessel A, Avshovich N, et al.: Clinical and laboratory parameters in predicting chronic urticaria duration: a prospective study of 139 patients. Allergy 2004, 59:869–873. Prospective study of clinical features in CIU related to disease duration. Federman DG, Kirsner RS, Moriarty JP, Concato J: The effect of antibiotic therapy for patients infected with Helicobacter pylori who have chronic urticaria. J Am Acad Dermatol 2003, 49:861–864. Wedi B, Raap U, Kapp A: Chronic urticaria and infections. Curr Opin Allergy Clin Immunol 2004, 4:387–396. Grattan CE, O’Donnell BF, Francis DM, et al.: Randomized double-blind study of cyclosporin in chronic "idiopathic" urticaria. Br J Dermatol 2000, 143:365–372. Beck L, Marcotte G, MacGlashan J, et al.: Omalizumab induced reductions in mast cell FceRI expression and function. J Allergy Clin Immunol 2004, 114:527–530. Tong LJ, Balakrishnan G, Kochan JP, et al.: Assessment of autoimmunity in patients with chronic urticaria. J Allergy Clin Immunol 1997, 99:461–465. Ferrer M, Kinet JP, Kaplan AP: Comparative studies of functional and binding assays for IgG anti-Fc(epsilon)RIalpha (alpha-subunit) in chronic urticaria. J Allergy Clin Immunol 1998, 101:672–676. Gruber BL, Baeza ML, Marchese MJ, et al.: Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. J Invest Dermatol 1988, 90:213–217. Hide M, Francis DM, Grattan CE, et al.: Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med 1993, 328:1599–1604. Grattan CE, Francis DM, Slater NG, et al.: Plasmapheresis for severe, unremitting, chronic urticaria. Lancet 1992, 339:1078–1080. Kikuchi Y, Kaplan AP: Mechanisms of autoimmune activation of basophils in chronic urticaria. J Allergy Clin Immunol 2001, 107:1056–1062. Kikuchi Y, Kaplan AP: A role for C5a in augmenting IgGdependent histamine release from basophils in chronic urticaria. J Allergy Clin Immunol 2002, 109:114–118. Niimi N, Francis DM, Kermani F, et al.: Dermal mast cell activation by autoantibodies against the high affinity IgE receptor in chronic urticaria. J Invest Dermatol 1996, 106:1001–1006. Schulman ES, Kagey-Sobotka A, MacGlashan DW Jr, et al.: Heterogeneity of human mast cells. J Immunol 1983, 131:1936–1941. Sabroe RA, Fiebiger E, Francis DM, et al.: Classification of anti-FcepsilonRI and anti-IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity. J Allergy Clin Immunol 2002, 110:492–499. Insight into relationship between serologic factors and CIU disease severity. Saini SS, Richardson JJ, Wofsy C, et al.: Expression and modulation of FcepsilonRIalpha and FcepsilonRIbeta in human blood basophils. J Allergy Clin Immunol 2001, 107:832–841. Fiebiger E, Hammerschmid F, Stingl G, Maurer D: Anti-FcepsilonRIalpha autoantibodies in autoimmune-mediated disorders. Identification of a structure-function relationship. J Clin Invest 1998, 101:243–251. Miescher SM, Horn MP, Pachlopnik JM, et al.: Natural anti-FcepsilonRIalpha autoantibodies isolated from healthy donors and chronic idiopathic urticaria patients reveal a restricted repertoire and autoreactivity on human basophils. Hum Antibodies 2001, 10:119–126. Sabroe RA, Poon E, Orchard GE, et al.: Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies. J Allergy Clin Immunol 1999, 103:484–493. Sabroe RA, Seed PT, Francis DM, et al.: Chronic idiopathic urticaria: comparison of the clinical features of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies. J Am Acad Dermatol 1999, 40:443–450. Grattan CE: Basophils in chronic urticaria. J Investig Dermatol Symp Proc 2001, 6:139–140. Grattan CE, Walpole D, Francis DM, et al.: Flow cytometric analysis of basophil numbers in chronic urticaria: basopenia is related to serum histamine releasing activity. Clin Exp Allergy 1997, 27:1417–1424. Kern F, Lichtenstein LM: Defective histamine release in chronic urticaria. J Clin Invest 1976, 57:1369–1377. Grattan CE, Dawn G, Gibbs S, Francis DM: Blood basophil numbers in chronic ordinary urticaria and healthy controls: diurnal variation, influence of loratadine and prednisolone and relationship to disease activity. Clin Exp Allergy 2003, 33:337–341. Sabroe RA, Francis DM, Barr RM, et al.: Anti-Fc(episilon)RI auto antibodies and basophil histamine releasability in chronic idiopathic urticaria. J Allergy Clin Immunol 1998, 102:651–658. Schleimer RP: Glucocorticosteroids: their mechanism of action and use in allergic diseases. In Allergy Principles and Practice, edn 4. Edited by Middleton E, Reed CE, Ellis EF, et al. St. Louis, MO: Mosby; 1993:893–925. Charlesworth EN, Kagey-Sobotka A, Schleimer RP, et al.: Prednisone inhibits the appearance of inflammatory mediators and the influx of eosinophils and basophils associated with the cutaneous late-phase response to allergen. J Immunol 1991, 146:671–676. Yoshimura C, Miyamasu M, Nagase H, et al.: Glucocorticoids induce basophil apoptosis. J Allergy Clin Immunol 2001, 108:215–220. Ying S, Kikuchi Y, Meng Q, et al.: TH1/TH2 cytokines and inflammatory cells in skin biopsy specimens from patients with chronic idiopathic urticaria: comparison with the allergen-induced late-phase cutaneous reaction. J Allergy Clin Immunol 2002, 109:694–700. Recent study defining characteristics of cellular infiltrate in CIU. Caproni M, Volpi W, Macchia D, et al.: Infiltrating cells and related cytokines in lesional skin of patients with chronic idiopathic urticaria and positive autologous serum skin test. Exp Dermatol 2003, 12:621–628. Smith CH, Kepley C, Schwartz LB, Lee TH: Mast cell number and phenotype in chronic idiopathic urticaria. J Allergy Clin Immunol 1995, 96:360–364. Caproni M, Giomi B, Volpi W, et al.: Chronic idiopathic urticaria: infiltrating cells and related cytokines in autologous serum-induced wheals. Clin Immunol 2005, 114:284–292. Schwartz LB, Sakai K, Bradford TR, et al.: The alpha form of human tryptase is the predominant type present in blood at baseline in normal subjects and is elevated in those with systemic mastocytosis. J Clin Invest 1995, 96:2702–2710. Asero R, Tedeschi A, Lorini M, et al.: Circulating stem cell factor in patients with chronic idiopathic urticaria. Ann Allergy Asthma Immunol 2003, 91:79–81. Kaplan AP, Garofalo J, Sigler R, Hauber T: Idiopathic cold urticaria: in vitro demonstration of histamine release upon challenge of skin biopsies. N Engl J Med 1981, 305:1074–1077. Irani AA, Schechter NM, Craig SS, et al.: Two types of human mast cells that have distinct neutral protease compositions. Proc Natl Acad Sci U S A 1986, 83:4464–4468. Jacques P, Lavoie A, Bedard PM, et al.: Chronic idiopathic urticaria: profiles of skin mast cell histamine release during active disease and remission. J Allergy Clin Immunol 1992, 89:1139–1143. Leung DY: Infection in atopic dermatitis. Curr Opin Pediatr 2003, 15:399–404. Supajatura V, Ushio H, Nakao A, et al.: Differential responses of mast cell Toll-like receptors 2 and 4 in allergy and innate immunity. J Clin Invest 2002, 109:1351–1359. Marshall JS, McCurdy JD, Olynych T: Toll-like receptor-mediated activation of mast cells: implications for allergic disease? Int Arch Allergy Immunol 2003, 132:87–97. Varadaradjalou S, Feger F, Thieblemont N, et al.: Toll-like receptor 2 (TLR2) and TLR4 differentially activate human mast cells. Eur J Immunol 2003, 33:899–906. Tkaczyk C, Okayama Y, Metcalfe DD, Gilfillan AM: Fcgamma receptors on mast cells: activatory and inhibitory regulation of mediator release. Int Arch Allergy Immunol 2004, 133:305–315. Blank U, Rivera J: The ins and outs of IgE-dependent mast-cell exocytosis. Trends Immunol 2004, 25:266–273. Conroy MC, Adkinson NF Jr, Lichtenstein LM: Measurement of IgE on human basophils: relation to serum IgE and anti-IgEinduced histamine release. J Immunol 1977, 118:1317–1321. Findlay SR, Lichtenstein LM: Basophil releasability in patients with asthma. Am Rev Respir Dis 1980, 122:53–59. Kepley CL, Youssef L, Andrews RP, et al.: Syk deficiency in nonreleaser basophils. J Allergy Clin Immunol 1999, 104:279–284. Lavens-Phillip S, MacGlashan D: The tyrosine kinases, p53 lyn, p72 syk are differentially expressed at the protein level, not the mRNA level in non-releasing human basophils. Am J Cell Respir Mol Med 2000, 23:566–571. Kepley CL, Cohen N: Evidence for human mast cell nonreleaser phenotype. J Allergy Clin Immunol 2003, 112:457–459. Huber M, Helgason CD, Damen JE, et al.: The src homology 2-containing inositol phosphatase (SHIP) is the gatekeeper of mast cell degranulation. Proc Natl Acad Sci U S A 1998, 95:11330–11335. Rauh MJ, Krystal G: Of mice and men: elucidating the role of SH2-containing inositol 5-phosphatase (SHIP) in human disease. Clin Invest Med 2002, 25:68–70. Excellent review of the clinical implications of SHIP phosphatase activity in human disease. MacDonald SM, Rafnar T, Langdon J, Lichtenstein LM: Molecular identification of an IgE-dependent histamine-releasing factor. Science 1995, 269:688–690. Vonakis BM, Gibbons S Jr, Sora R, et al.: Src homology 2 domain-containing inositol 5’ phosphatase is negatively associated with histamine release to human recombinant histamine-releasing factor in human basophils. J Allergy Clin Immunol 2001, 108:822–831. Clement S, Krause U, Desmedt F, et al.: The lipid phosphatase SHIP2 controls insulin sensitivity. Nature 2001, 409:92–97. Marion E, Kaisaki PJ, Pouillon V, et al.: The gene INPPL1, encoding the lipid phosphatase SHIP2, is a candidate for type 2 diabetes in rat and man. Diabetes 2002, 51:2012–2017. Saini SS, Vasagar K, Huang F, et al.: Signaling defects in basophils in chronic urticaria. J Allergy Clin Immunol 2003, 111:S178.