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1
Requirement for CD4+ cells in resistance to Pneumocystis carinii pneumonia in mice.小鼠对卡氏肺孢子虫肺炎抵抗力中CD4 + 细胞的需求
J Exp Med. 1990 Sep 1;172(3):937-45. doi: 10.1084/jem.172.3.937.
2
CD40 ligand is required for resolution of Pneumocystis carinii pneumonia in mice.CD40配体是小鼠卡氏肺孢子虫肺炎消退所必需的。
J Immunol. 1995 Oct 1;155(7):3525-9.
3
T cells are not sufficient for resistance to Pneumocystis carinii pneumonia in mice.T细胞对于小鼠抵抗卡氏肺孢子虫肺炎并不充分。
J Protozool. 1991 Nov-Dec;38(6):44S-45S.
4
Sensitized CD8+ T cells fail to control organism burden but accelerate the onset of lung injury during Pneumocystis carinii pneumonia.致敏的CD8 + T细胞无法控制机体负荷,但会加速卡氏肺孢子虫肺炎期间肺损伤的发生。
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5
Resolution of Pneumocystis carinii pneumonia in CD4+ lymphocyte-depleted mice given aerosols of heat-treated Escherichia coli.给予经热处理的大肠杆菌气雾剂的CD4 +淋巴细胞耗竭小鼠中卡氏肺孢子虫肺炎的消退
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6
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7
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8
Both immunity and hyperresponsiveness to Pneumocystis carinii result from transfer of CD4+ but not CD8+ T cells into severe combined immunodeficiency mice.对卡氏肺孢子虫的免疫和高反应性均源于将CD4 +而非CD8 + T细胞转移至严重联合免疫缺陷小鼠体内。
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9
Neonatal T cells in an adult lung environment are competent to resolve Pneumocystis carinii pneumonia.成年肺部环境中的新生儿T细胞有能力解决卡氏肺孢子虫肺炎。
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Delayed inflammatory response to Pneumocystis carinii infection in neonatal mice is due to an inadequate lung environment.新生小鼠对卡氏肺孢子虫感染的延迟性炎症反应是由于肺部环境不足所致。
J Immunol. 2000 Dec 1;165(11):6480-6. doi: 10.4049/jimmunol.165.11.6480.

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7
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The Trophic Life Cycle Stage of the Opportunistic Fungal Pathogen Pneumocystis murina Hinders the Ability of Dendritic Cells To Stimulate CD4 T Cell Responses.机会性真菌病原体鼠肺孢子菌的营养生命周期阶段阻碍了树突状细胞刺激CD4 T细胞反应的能力。
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9
Pulmonary Interleukin-17-Positive Lymphocytes Increase during Pneumocystis murina Infection but Are Not Required for Clearance of Pneumocystis.在鼠肺孢子菌感染期间,肺部白细胞介素-17阳性淋巴细胞增多,但清除肺孢子菌并不需要它们。
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10
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Immune responses after localized lung immunization in the dog.犬局部肺免疫后的免疫反应。
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The mechanism of appearance of specific antibody-forming cells in lungs of inbred mice after intratracheal immunization with sheep erythrocytes.用绵羊红细胞经气管内免疫近交系小鼠后,其肺中特异性抗体形成细胞出现的机制。
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Effect of T-cell transfer on Pneumocystis carinii infection in nude mice.T细胞转移对裸鼠卡氏肺孢子虫感染的影响。
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NHLBI workshop summary. Pulmonary complications of the acquired immunodeficiency syndrome: an update. Report of the second National Heart, Lung and Blood Institute workshop.美国国立心肺血液研究所研讨会总结。获得性免疫缺陷综合征的肺部并发症:最新情况。第二次国立心肺血液研究所研讨会报告。
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Attachment of Pneumocystis carinii to rat pneumocytes.卡氏肺孢子虫与大鼠肺细胞的附着。
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Role of alveolar macrophages in lipopolysaccharide-induced neutrophil accumulation.肺泡巨噬细胞在脂多糖诱导的中性粒细胞聚集中的作用。
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小鼠对卡氏肺孢子虫肺炎抵抗力中CD4 + 细胞的需求

Requirement for CD4+ cells in resistance to Pneumocystis carinii pneumonia in mice.

作者信息

Harmsen A G, Stankiewicz M

机构信息

Trudeau Institute, Inc., Saranac Lake, New York 12983.

出版信息

J Exp Med. 1990 Sep 1;172(3):937-45. doi: 10.1084/jem.172.3.937.

DOI:10.1084/jem.172.3.937
PMID:2117637
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2188525/
Abstract

The importance of CD4+ cells in resistance to Pneumocystis carinii (PC) in PC-susceptible severe combined immunodeficient (SCID) mice that were made resistant to PC by immunocompetent spleen cell transfer, and in conventional PC-resistant mice, was investigated. SCID mice with naturally acquired PC pneumonia (PCP) were given infusions of spleen cells from immunocompetent donors. This reconstitution caused the recipients to resolve their PCP. Treatment of reconstituted SCID mice with anti-CD4 monoclonal antibodies (mAbs) to deplete them of CD4+ cells eliminated their ability to resolve PCP, whereas treating them with anti-CD8 mAb to deplete CD8+ cells had no effect. The findings indicate, therefore, that resistance to PCP in immunologically reconstituted SCID mice is dependent on CD4+ cells. To determine whether CD4+ cells enable conventional mice to resist PCP, B6D2 mice were treated with anti-CD4 mAb to deplete them of CD4+ cells in an attempt to induce PCP. After 10-11 wk of treatment, these mice developed progressive PCP. Taken together, these results indicate that loss of CD4+ cells predisposes mice to PC infection.

摘要

研究了CD4 +细胞在易患卡氏肺孢子虫(PC)的严重联合免疫缺陷(SCID)小鼠中对PC的抗性的重要性,这些SCID小鼠通过免疫活性脾细胞转移对PC产生抗性,同时也研究了其在常规抗PC小鼠中的重要性。给患有自然获得性PC肺炎(PCP)的SCID小鼠输注来自免疫活性供体的脾细胞。这种重建使受体小鼠的PCP得到缓解。用抗CD4单克隆抗体(mAb)处理重建的SCID小鼠以耗尽其CD4 +细胞,消除了它们缓解PCP的能力,而用抗CD8 mAb处理以耗尽CD8 +细胞则没有效果。因此,这些发现表明,免疫重建的SCID小鼠对PCP的抗性取决于CD4 +细胞。为了确定CD4 +细胞是否使常规小鼠能够抵抗PCP,用抗CD4 mAb处理B6D2小鼠以耗尽其CD4 +细胞,试图诱导PCP。经过10 - 11周的治疗,这些小鼠发展为进行性PCP。综上所述,这些结果表明CD4 +细胞的缺失使小鼠易患PC感染。