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1
Inflammatory lymphoid cells. Cells in immunized lymph nodes that move to sites of inflammation.炎性淋巴细胞。存在于免疫淋巴结中并迁移至炎症部位的细胞。
Immunology. 1972 Mar;22(3):493-502.
2
Contact sensitivity in the mouse. IX. The role of immunological and non-immunological inflammation in the movement of lymphocytes to immunized lymph nodes.小鼠的接触敏感性。IX. 免疫性和非免疫性炎症在淋巴细胞向免疫淋巴结迁移中的作用。
Immunology. 1973 May;24(5):885-94.
3
Depression of delayed hypersensitivity by pretreatment with Freund-type adjuvants. 3. Depressed arrival of lymphoid cells at recently immunized lymph nodes in mice pretreated with adjuvants.用弗氏佐剂预处理对迟发型超敏反应的抑制作用。3. 佐剂预处理小鼠中淋巴细胞到达近期免疫淋巴结的情况受到抑制。
Clin Exp Immunol. 1972 Aug;11(4):579-84.
4
Cytotoxicity of immune guinea-pig cells. I. Investigation of a correlation with delayed hypersensitivity and a comparison of cytotoxicity of spleen, lymph node and peritoneal exudate cells.免疫豚鼠细胞的细胞毒性。I. 与迟发型超敏反应相关性的研究以及脾细胞、淋巴结细胞和腹腔渗出细胞细胞毒性的比较。
Immunology. 1972 Oct;23(4):559-67.
5
The fate of antigen in induction of delayed allergic responses.抗原在迟发型过敏反应诱导中的命运。
Adv Biol Skin. 1971;11:63-93.
6
Morphologic changes in draining lymph nodes and in lymphocyte cultures after sensitization with complete or incomplete Freund's adjuvant. Correlation with immunologic events in vivo and in culture.用完全或不完全弗氏佐剂致敏后引流淋巴结及淋巴细胞培养物中的形态学变化。与体内及培养中的免疫事件的相关性。
J Immunol. 1971 Aug;107(2):422-35.
7
The origin of mononuclear cells in delayed hypersensitivity reactions.迟发型超敏反应中单核细胞的起源。
Ann Inst Pasteur (Paris). 1969 May;116(5):575-8.
8
The allogeneic effect: increased cellular immune and inflammatory responses.同种异体效应:增强细胞免疫和炎症反应。
J Immunol. 1974 Jun;112(6):2166-75.
9
Contact and delayed hypersensitivity in the mouse. I. Active sensitization and passive transfer.小鼠的接触性和迟发型超敏反应。I. 主动致敏和被动转移。
Immunology. 1968 Sep;15(3):405-16.
10
Contact sensitivity in the mouse. XI. Movement of T blasts in the draining lymph nodes to sites of inflammation.小鼠中的接触敏感性。十一、引流淋巴结中T母细胞向炎症部位的移动。
Immunology. 1973 Sep;25(3):485-94.

引用本文的文献

1
Studies of efferent lymph cells from nodes stimulated with oxazolone.对用恶唑酮刺激的淋巴结的传出淋巴细胞的研究。
Immunology. 1980 Feb;39(2):141-9.
2
Changes in lymphocyte adhesiveness during contact sensitization.接触致敏过程中淋巴细胞黏附性的变化。
Br J Exp Pathol. 1981 Apr;62(2):158-64.
3
Induction of immunological memory in the skin. Role of local T cell retention.皮肤中免疫记忆的诱导。局部T细胞滞留的作用。
Clin Exp Immunol. 1983 Jan;51(1):141-8.
4
Comparative migration of T- and B-lymphocyte subpopulations into skin inflammatory sites.T淋巴细胞亚群和B淋巴细胞亚群向皮肤炎症部位的比较性迁移。
Immunology. 1983 Mar;48(3):519-27.
5
Viruses and demyelinating disease of the central nervous system.病毒与中枢神经系统脱髓鞘疾病
Neurol Clin. 1983 Aug;1(3):681-700. doi: 10.1016/S0733-8619(18)31143-5.
6
Flare-up of antigen-induced arthritis in mice after challenge with intravenous antigen: studies on the characteristics of and mechanisms involved in the reaction.静脉注射抗原激发后小鼠抗原诱导性关节炎的复发:关于该反应特征及相关机制的研究
Clin Exp Immunol. 1984 Feb;55(2):287-94.
7
Contact sensitivity in the mouse. XII. The use of DNA synthesis in vivo to determine the anatomical location of immunological unresponsiveness to picryl chloride.小鼠中的接触性敏感。十二、利用体内DNA合成来确定对苦味酰氯免疫无反应性的解剖学位置。
Immunology. 1973 Sep;25(3):495-508.
8
Interaction between contact sensitizing agents and sensitized lymph node cells in mice.小鼠中接触致敏剂与致敏淋巴结细胞之间的相互作用。
Immunology. 1973 Jul;25(1):111-21.
9
Contact sensitivity in the mouse. IX. The role of immunological and non-immunological inflammation in the movement of lymphocytes to immunized lymph nodes.小鼠的接触敏感性。IX. 免疫性和非免疫性炎症在淋巴细胞向免疫淋巴结迁移中的作用。
Immunology. 1973 May;24(5):885-94.
10
Classification of immunological unresponsiveness and tolerance.免疫无反应性与耐受性的分类。
Proc R Soc Med. 1973 May;66(5):468-71. doi: 10.1177/003591577306600524.

本文引用的文献

1
A HISTOLOGICAL AND AUTORADIOGRAPHIC STUDY OF LYMPH NODES DURING THE DEVELOPMENT OF CONTACT SENSITIVITY IN THE GUINEA-PIG.豚鼠接触性敏感发育过程中淋巴结的组织学与放射自显影研究
Br J Exp Pathol. 1965 Apr;46(2):147-54.
2
CELLULAR SPECIFICITY IN THE HOMOGRAFT REACTION.同种移植反应中的细胞特异性
J Exp Med. 1964 Mar 1;119(3):377-88. doi: 10.1084/jem.119.3.377.
3
Distribution of allogeneic 51Cr-labelled lymph node cells in mice.同种异体51Cr标记的淋巴结细胞在小鼠体内的分布。
Transplantation. 1966 Mar;4(2):138-53. doi: 10.1097/00007890-196603000-00003.
4
The mediator of cellular immunity. 3. Lymphocyte traffic from the blood into the inflamed peritoneal cavity.细胞免疫的介质。3. 淋巴细胞从血液进入炎症性腹膜腔的游走。
J Exp Med. 1971 Apr 1;133(4):864-76. doi: 10.1084/jem.133.4.864.
5
Induction and recall in contact sensivitity. Changes in skin and draining lymph nodes of intact and thymectomized mice.接触敏感性中的诱导和回忆。完整小鼠和胸腺切除小鼠的皮肤及引流淋巴结的变化。
J Exp Med. 1969 Oct 1;130(4):671-90. doi: 10.1084/jem.130.4.671.
6
Studies of the cells in the afferent and efferent lymph of lymph nodes draining the site of skin homografts.对引流皮肤同种异体移植部位的淋巴结的输入淋巴管和输出淋巴管中的细胞进行的研究。
J Exp Med. 1967 May 1;125(5):737-54. doi: 10.1084/jem.125.5.737.
7
Polysaccharide in delayed hypersensitivity. I. Pneumococcal polysaccharide as inducer and elicitor of delayed reactivity in guinea pigs.迟发型超敏反应中的多糖。I. 肺炎球菌多糖作为豚鼠迟发型反应的诱导剂和激发剂。
J Exp Med. 1970 Jan 1;131(1):189-206. doi: 10.1084/jem.131.1.189.
8
The influence of the cellular infiltrate on the evolution and intensity of delayed hypersensitivity reactions.细胞浸润对迟发型超敏反应的演变及强度的影响。
J Exp Med. 1969 Feb 1;129(2):363-70. doi: 10.1084/jem.129.2.363.
9
Studies on the origin and reactive ability in vivo of peritoneal exudate cells in delayed hypersensitivity.迟发型超敏反应中腹膜渗出细胞的体内起源及反应能力的研究
Int Arch Allergy Appl Immunol. 1967;31(4):403-16. doi: 10.1159/000229886.
10
The role of immunoglobulins in lymphocyte-mediated cell damage, in vitro. I. Comparison of the effects of target cell specific antibody and normal serum factors on cellular damage by immune and non-immune lymphocytes.免疫球蛋白在体外淋巴细胞介导的细胞损伤中的作用。I. 靶细胞特异性抗体和正常血清因子对免疫和非免疫淋巴细胞所致细胞损伤影响的比较。
Immunology. 1970 Mar;18(3):397-404.

炎性淋巴细胞。存在于免疫淋巴结中并迁移至炎症部位的细胞。

Inflammatory lymphoid cells. Cells in immunized lymph nodes that move to sites of inflammation.

作者信息

Asherson G L, Allwood G G

出版信息

Immunology. 1972 Mar;22(3):493-502.

PMID:4402113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1407785/
Abstract

The arrival of cells from normal and immunized lymph node cells at sites of inflammation was studied. Mice were immunized with oxazolone' or picryl chloride and 3–4 days later the draining lymph node cells were dissociated, labelled with Cr and injected intravenously into recipients. Sites of inflammation were produced in the recipients by painting the ear with chemically reactive contact sensitizing agents or croton oil. The net arrival of normal lymph node cells at sites of inflammation was 0.1 per cent. In contrast the arrival of cells from immunized lymph nodes was 4–8 times greater. The peak number of cells that moved to sites of inflammation occurred 4 days after immunization with oxazolone'. An increase in the percentage of cells that moved to sites of inflammation occurred in lymph nodes after immunization with a number of agents including contact sensitizing agents, skin grafts and Freund's complete adjuvant. There was little or no increase in mice rendered unresponsive to picryl chloride and then immunized with picryl chloride or in mice injected with aluminium hydroxide, alum precipitated mouse serum or pneumococcal polysaccharide. This suggested that immunization and possibly the induction of delayed hypersensitivity was necessary for the generation of these cells. The arrival of the cells did not depend on antigenic similarity between the agent used to immunize the lymph node and the agent used to produce inflammation. For example increased arrival of cells from immunized lymph nodes occurred at sites of inflammation produced in the ear by croton oil or in the peritoneal cavity by paraffin oil.

摘要

研究了正常和免疫的淋巴结细胞到达炎症部位的情况。用恶唑酮或苦味酰氯对小鼠进行免疫,3 - 4天后分离引流淋巴结细胞,用铬标记后静脉注射到受体小鼠体内。通过用化学反应性接触致敏剂或巴豆油涂抹耳朵在受体小鼠中产生炎症部位。正常淋巴结细胞到达炎症部位的净迁移率为0.1%。相比之下,免疫淋巴结细胞的迁移率要高4 - 8倍。用恶唑酮免疫后4天,迁移到炎症部位的细胞数量达到峰值。在用包括接触致敏剂、皮肤移植和弗氏完全佐剂在内的多种试剂免疫后,淋巴结中迁移到炎症部位的细胞百分比增加。在用苦味酰氯致敏后再用苦味酰氯免疫的小鼠或注射氢氧化铝、明矾沉淀的小鼠血清或肺炎球菌多糖的小鼠中,迁移到炎症部位的细胞几乎没有增加或没有增加。这表明免疫以及可能的迟发型超敏反应的诱导对于这些细胞的产生是必要的。细胞的迁移并不取决于用于免疫淋巴结的试剂与用于产生炎症的试剂之间的抗原相似性。例如,来自免疫淋巴结的细胞在由巴豆油在耳朵产生的炎症部位或由石蜡油在腹腔产生的炎症部位的迁移增加。