IFN-γ-independent IgG2a production in mice infected with viruses and parasites
IFN-γ-independent IgG2a production in mice infected with viruses and parasites
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DOI：
10.1093/intimm/12.2.223
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发表时间：
2000-02-01
影响因子：
4.4
通讯作者：
Coutelier, JP
中科院分区：
文献类型：
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作者：
Markine-Goriaynoff, D;van der Logt, JTM;Coutelier, JP
在感染某些病毒和细胞内寄生虫后，抗体的产生仅限于IgG2a。我们首先观察到，乳酸脱氢酶升高病毒（LDV）或小鼠腺病毒等活病毒主要诱导IgG2a反应，而针对被杀死病毒产生的大部分抗体是IgG1，当将活病毒粒子加入灭活病毒颗粒时，这种IgG1抗病毒反应被抑制。这些结果表明，IgG2a的优势与感染过程本身有关，而不是与所涉及的抗原类型有关。由于已知ifn - γ可以通过活化的B淋巴细胞刺激IgG2a的产生，并在感染后分泌，因此我们研究了该细胞因子在LDV引起的抗体同型分布中的作用。在缺乏ifn - γ受体或使用抗ifn - γ抗体治疗的小鼠中，大多数IgG2a反应相对不受影响。弓形虫和克氏锥虫感染寄生虫后也有类似的不依赖ifn - γ的IgG2a分泌，但感染引发的不依赖ifn - γ的IgG2a分泌仍然需要功能性T-h淋巴细胞的存在。因此，ifn - γ分泌以外的信号可以解释病毒和寄生虫引发的抗体分泌中t -h依赖的同型偏倚。
\After infection with some viruses and intracellular parasites, antibody production is restricted to IgG2a. We first observed that, whereas live viruses such as lactate dehydrogenase-elevating virus (LDV) or mouse adenovirus induced mostly an IgG2a response, a large proportion of antibodies produced against killed viruses were IgG1, This IgG1 antiviral response was suppressed when live virions were added to inactivated viral particles. These results indicate that the IgG2a preponderance is related to the infectious process itself rather than to the type of antigen involved. Since IFN-gamma is known to stimulate IgG2a production by activated B lymphocytes and to be secreted after infection, we examined the role of this cytokine in the antibody isotypic distribution caused by LDV. Most IgG2a responses were relatively unaffected in mice deficient for the IFN-gamma receptor or treated with anti-IFN-gamma antibody. A similar IFN-gamma-independent IgG2a secretion was observed after infection with the parasites Toxoplasma gondii and Trypanosoma cruzi, However, the IFN-gamma-independent IgG2a production triggered by infection still required the presence of functional T-h lymphocytes. Therefore, signal(s) other than IFN-gamma secretion may explain the T-h-dependent isotypic bias in antibody secretion triggered by viruses and parasites.