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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >CD47-deficient mice have decreased production of intestinal IgA following oral immunization but a maintained capacity to induce oral tolerance
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CD47-deficient mice have decreased production of intestinal IgA following oral immunization but a maintained capacity to induce oral tolerance

机译：CD47缺陷型小鼠口服免疫后肠道IgA产量降低，但诱导口服耐受的能力得以维持

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Signal regulatory protein α (SIRPα/CD172a), expressed by myeloid cells including CD11b + dendritic cells, interacts with ubiquitously expressed CD47 to mediate cell-cell signalling and therefore, may be pivotal in the development of tolerance or immunity. We show that in mice deficient in CD47 (CD47 -/-) the cellularity in gut-associated lymphoid tissues is reduced by 50%. In addition, the frequency of CD11b +CD172a + dendritic cells is significantly reduced in the gut and mesenteric lymph nodes, but not in Peyer's patches. Activation of ovalbumin (OVA)-specific CD4 + T cells in the mesenteric lymph nodes after feeding OVA is reduced in CD47 -/- mice compared with wild-type however, induction of oral tolerance is maintained. The addition of cholera toxin generated normal serum anti-OVA IgG and IgA titres but resulted in reduced intestinal anti-OVA IgA in CD47 -/- mice. Replacing the haematopoietic compartment in CD47 -/- mice with wild-type cells restored neither the cellularity in gut-associated lymphoid tissues nor the capacity to produce intestinal anti-OVA IgA following immunization. This study demonstrates that CD47 signalling is dispensable for oral tolerance induction, whereas the expression of CD47 by non-haematopoietic cells is required for intestinal IgA B-cell responses. This suggests that differential CD4 T cell functions control tolerance and enterotoxin-induced IgA immunity in the gut.
机译：由包括CD11b +树突状细胞在内的髓样细胞表达的信号调节蛋白α（SIRPα/ CD172a）与普遍表达的CD47相互作用，介导细胞信号传导，因此可能在耐受性或免疫性发展中起关键作用。我们显示，在缺乏CD47（CD47-/-）的小鼠中，肠道相关淋巴组织的细胞减少了50％。此外，在肠道和肠系膜淋巴结中，CD11b + CD172a +树突状细胞的频率显着降低，而在Peyer's斑中则没有。与野生型相比，CD47-/-小鼠在饲喂OVA后肠系膜淋巴结中卵清蛋白（OVA）特异性CD4 + T细胞的激活减少，但是，维持了对口腔耐受的诱导。添加霍乱毒素可产生正常的血清抗OVA IgG和IgA滴度，但导致CD47-/-小鼠肠道抗OVA IgA降低。用野生型细​​胞代替CD47-/-小鼠的造血区室，既不恢复肠道相关淋巴组织的细胞活力，也不恢复免疫后产生肠道抗OVA IgA的能力。这项研究表明CD47信号传导对于口服耐受诱导是必不可少的，而非造血细胞表达CD47是肠道IgA B细胞应答所必需的。这表明差异的CD4 T细胞功能控制肠道的耐受性和肠毒素诱导的IgA免疫力。

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