Tong L J, Balakrishnan G, Kochan J P, Kinét J P, Kaplan A P
Department of Medicine, State University of New York at Stony Brook 11794-8161, USA.
J Allergy Clin Immunol. 1997 Apr;99(4):461-5. doi: 10.1016/s0091-6749(97)70071-x.
The etiology of chronic urticaria is unknown, and an exogenous allergen cannot be identified as the cause in the vast majority of subjects. Thus the concept has evolved that it might be autoimmune.
We have prospectively assessed sera obtained from 50 consecutive patients with chronic urticaria for the presence of autoantibodies that could be pathogenic.
We tested sera for their ability to release histamine from human basophils and to activate rat basophil leukemia cells that were transfected with the alpha subunit of the IgE receptor. We also tested selected sera for anti-IgE antibodies and for IgG anti-Fc epsilon RI alpha by Western blot.
Sera from 38 of 50 patients with chronic urticaria released beta-hexosaminidase from transfected rat basophil leukemia cells, whereas only one of 20 control sera did so (p < 0.001); in 30 subjects this could be attributed to IgG anti- Fc epsilon RI alpha. When human basophils were used, sera from 20 of 50 patients with chronic urticaria released a significant quantity of histamine compared with one of 20 control subjects (p < 0.01). Six patients with chronic urticaria and one control subject had IgG anti-IgE. In selected sera we could demonstrate IgG anti-Fc epsilon RI alpha by Western blot; however, some sera are positive for histamine release but do not demonstrate such binding.
A large fraction of patients with chronic urticaria have antibody directed to Fc epsilon RI alpha that is functional (60%). A smaller number have IgG anti-IgE (10%). A third group may also have circulating factors capable of activating basophils or mast cells of which the identity is unknown. Thus chronic urticaria may be autoimmune in origin.
慢性荨麻疹的病因不明，绝大多数患者无法确定外源性过敏原为病因。因此，其病因可能是自身免疫性的这一概念逐渐形成。
我们前瞻性地评估了连续50例慢性荨麻疹患者血清中可能具有致病性的自身抗体。
我们检测了血清从人嗜碱性粒细胞释放组胺以及激活转染了IgE受体α亚基的大鼠嗜碱性粒细胞白血病细胞的能力。我们还通过蛋白质印迹法检测了选定血清中的抗IgE抗体和IgG抗FcεRIα。
50例慢性荨麻疹患者中有38例的血清可使转染的大鼠嗜碱性粒细胞白血病细胞释放β-己糖胺酶，而20例对照血清中只有1例可使细胞释放该酶（p<0.001）；在30名受试者中，这可归因于IgG抗FcεRIα。使用人嗜碱性粒细胞时，50例慢性荨麻疹患者中有20例的血清释放出大量组胺，而20名对照受试者中只有1例出现这种情况（p<0.01）。6例慢性荨麻疹患者和1名对照受试者有IgG抗IgE。在选定的血清中，我们通过蛋白质印迹法可检测到IgG抗FcεRIα；然而，一些血清组胺释放呈阳性，但未显示出此类结合。
很大一部分慢性荨麻疹患者有针对FcεRIα的功能性抗体（60%）。少数患者有IgG抗IgE（10%）。第三组患者可能也有能够激活嗜碱性粒细胞或肥大细胞的循环因子，其性质尚不清楚。因此，慢性荨麻疹可能起源于自身免疫。
