流感嗜血杆菌血清群b型鉴定

广州健仑生物科技有限公司

我司还有很多种血清学诊断血清、血液检测、免疫检测产品、毒素检测、凝集检测、酶免检测、层析检测、免疫荧光检测产品，。

（ MOB：杨永汉）

【流感知识】

流感嗜血杆菌是一种没有运动力的革兰氏阴性杆菌。它是于1892年由费佛博士在流行性感冒的瘟疫中发现。它一般都是好氧生物，但可以成长为兼性厌氧生物。
流感嗜血杆菌zui初被误认为是流行性感冒的病因，但直至1933年，当发现流行性感冒的病毒性病原后，才消除了这种误解。不过，流感嗜血杆菌仍会导致其他不同种类的病症。  

本试剂盒主要用于对病菌细菌进行检测，利用快速玻片凝集检测技术

嗜血杆菌属血清群A型鉴定

嗜血杆菌属血清群A型鉴定

嗜血杆菌属血清群A型鉴定

嗜血杆菌属血清群A型鉴定

流感嗜血杆菌A/B型凝集抗血清Haemophilus

流感嗜血杆菌A/B型凝集抗血清Haemophilus

流感嗜血杆菌A/B/C型血清群

流感嗜血杆菌A/B/C型血清群

流感嗜血杆菌A/B/C3型凝集抗血清

流感嗜血杆菌A/B/C3型凝集抗血清

a型流感嗜血杆菌诊断血清

a型流感嗜血杆菌诊断血清

玻片凝集法鉴定流感嗜血杆菌

玻片凝集法鉴定流感嗜血杆菌

b型2ml流感嗜血杆菌快速玻片法检测血清

b型2ml流感嗜血杆菌快速玻片法检测血清

A型、B型流感嗜血杆菌多群血清

A型、B型流感嗜血杆菌多群血清

流感嗜血杆菌血清群b型鉴定

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【公司名称】 广州健仑生物科技有限公司
【市场部】    杨永汉

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【腾讯  】 
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-103

有证据 提示本病存在免疫调节异常。本病的含IgA1循环免疫复合物中， 发现有多聚的IgA1类风湿因子；抗α重链Fab片断的IgG抗体增多 而IgM抗体减少。有趣的是HIV感染者也存在类似的抗免疫球蛋白 模式，却不发生肾脏IgA沉积。这证明单单这些循环的自身抗体存 在，并不是系膜IgA沉积的原因。此外目前还发现了二种抗内皮细 胞的自身抗体（属IgG）。本病肾组织中常有C3沉积，提示激活了 补体旁路途径。然而IgA本身无激活补体的能力，IgA免疫复合物 虽可激活补体旁路途径，但它结合补体和C3b的能力很弱。通常认 为在肾脏发生补体激活和形成膜攻击复合物，需有IgG-IgA复合物 ，但是本病肾组织中有IgA和C3沉积而没有IgG或IgM沉积却很常见 。因此，本病补体激活的机制尚不清楚。细胞免疫也参与了发病 机制。已发现本病可有T辅助细胞（CD4）增加和T抑制细胞（CD8 ）减少；具有转换IgM合成为IgA合成的Ta4细胞增加，与之有关的 Sa1等位基因的频度也增加；引起IgA同型转换的TGFβ、促进产生 IgA的B淋巴细胞分化的IL-5和介导IgA产生的IL-4形成均有增加 。虽然T细胞和B细胞均参与了增加IgA合成的过程，但IgA合成增 多并不是系膜区IgA沉积的原因，因为在IgA多发性骨髓瘤病人中 罕见有组织IgA沉积。因此，结构-免疫学/理化异常才可能是系膜 IgA沉积的原因。
Evidence suggests that there is an immunoregulatory abnormality in this disease. Among the IgA1 circulating immune complexes of this disease, polyvalent IgA1 rheumatoid factor was found; the IgG antibody against the α heavy chain Fab fragment increased while the IgM antibody decreased. Interestingly, HIV-infected persons also have similar anti-immunoglobulin patterns but no renal IgA deposition. This proves that these circulating autoantibodies alone are not responsible for the deposition of mesangial IgA. In addition, two anti-endothelial autoantibodies (genus IgG) have been discovered. C3 deposition often occurs in the renal tissue of this disease, suggesting activation of the complement alternative pathway. However, IgA itself has no ability to activate complement. IgA immune complexes can activate the complement alternative pathway, but its ability to bind complement and C3b is weak. It is generally believed that IgG-IgA complexes are required for complement activation and membrane attack complexes in the kidney, but it is common for the disease to have IgA and C3 deposition but no IgG or IgM deposition. Therefore, the mechanism of complement activation in this disease is not yet clear. Cellular immunity also participates in the pathogenesis. It has been found that the disease may have increased T-helper (CD4) and T-suppressor (CD8) cells; the number of Ta4 cells synthesized by converting IgM synthesis to IgA increases, and the frequency of Sa1 alleles associated therewith also increases; causing IgA Isotype-transformed TGFβ, IL-5 that promotes IgA-producing B lymphocyte differentiation, and IL-4 formation that mediates IgA production are all increased. Although both T and B cells are involved in the process of increasing IgA synthesis, increased IgA synthesis is not responsible for IgA deposition in the mesangial area because of the rare tissue IgA deposition in IgA patients with multiple myeloma. Therefore, structural-immunological/physicochemical abnormalities may be responsible for the deposition of mesangial IgA.