Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.65
M. Jensen, Ilona Nln, T. Iwamoto, Jessica M. Dorschner, D. Vsetecka, Gabrielle A McCoy, J. L. Paredes, T. Niewold
{"title":"1005 Characterization of regulatory receptors on plasmacytoid dendritic cells in lupus","authors":"M. Jensen, Ilona Nln, T. Iwamoto, Jessica M. Dorschner, D. Vsetecka, Gabrielle A McCoy, J. L. Paredes, T. Niewold","doi":"10.1136/lupus-2022-lupus21century.65","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.65","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42742428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.66
Nicholas L. Li, D. Birmingham, L. Biederman, T. Nadasdy, B. Rovin
{"title":"1101 Urine complement activation products in lupus nephritis","authors":"Nicholas L. Li, D. Birmingham, L. Biederman, T. Nadasdy, B. Rovin","doi":"10.1136/lupus-2022-lupus21century.66","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.66","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46054849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.67
A. Malvar, V. Alberton, Bruno J Lococo, M. C. Lourenço, Joaquín Martínez, Mauro Elencwajg, H. Nagaraja, B. Rovin
{"title":"1102 The trajectory of glomerular and tubulointerstitial lesions after treatment of lupus nephritis","authors":"A. Malvar, V. Alberton, Bruno J Lococo, M. C. Lourenço, Joaquín Martínez, Mauro Elencwajg, H. Nagaraja, B. Rovin","doi":"10.1136/lupus-2022-lupus21century.67","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.67","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43394669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-12-01DOI: 10.1136/lupus-2022-lupus21century.70
Vinh Phu Nguyen, A. Tatomir, C. Drachenberg, H. Rus, V. Rus
{"title":"1105 Response Gene to Complement-32 expression is upregulated in the kidney and promotes renal fibrosis in lupus nephritis","authors":"Vinh Phu Nguyen, A. Tatomir, C. Drachenberg, H. Rus, V. Rus","doi":"10.1136/lupus-2022-lupus21century.70","DOIUrl":"https://doi.org/10.1136/lupus-2022-lupus21century.70","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":" ","pages":""},"PeriodicalIF":3.2,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42259334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-01DOI: 10.1177/17534259221123309
Osama Abdel-Razek, Jason Audlin, Dennis S Poe, Guirong Wang
Otitis media (OM) is the most common disease among young children and one of the most frequent reasons to visit the pediatrician. Development of OM requires nasopharyngeal colonization by a pathogen which must gain access to the tympanic cavity through the eustachian tube (ET) along with being able to overcome the defense mechanisms of the immune system and middle ear mucosa. OM can be caused by viral or bacterial infection. The three main bacterial pathogens are Streptococcus pneumoniae, nontypeable Haemophilus influenzae (NTHi), and Moraxella catarrhalis. Innate immunity is important in OM resolution as the disease occurs in very young children before the development of specific immunity. Elements of innate immunity include natural barriers and pattern recognition receptors such as Toll like receptors (TLRs), and Nod like receptors (NLRs). Surfactant proteins A (SP-A) and D (SP-D) act as pattern recognition receptors and are found in the lung and many other tissues including the ET and the middle ear where they probably function in host defense. Surfactant has a potential for use in the treatment of OM due to surface tension lowering function in the ET, and the possible immune functions of SP-D and SP-A in the middle ear and ET.
{"title":"Surfactant proteins and innate immunity of otitis media.","authors":"Osama Abdel-Razek, Jason Audlin, Dennis S Poe, Guirong Wang","doi":"10.1177/17534259221123309","DOIUrl":"https://doi.org/10.1177/17534259221123309","url":null,"abstract":"<p><p>Otitis media (OM) is the most common disease among young children and one of the most frequent reasons to visit the pediatrician. Development of OM requires nasopharyngeal colonization by a pathogen which must gain access to the tympanic cavity through the eustachian tube (ET) along with being able to overcome the defense mechanisms of the immune system and middle ear mucosa. OM can be caused by viral or bacterial infection. The three main bacterial pathogens are <i>Streptococcus pneumoniae</i>, <i>nontypeable Haemophilus influenzae</i> (NTHi), and <i>Moraxella catarrhalis.</i> Innate immunity is important in OM resolution as the disease occurs in very young children before the development of specific immunity. Elements of innate immunity include natural barriers and pattern recognition receptors such as Toll like receptors (TLRs), and Nod like receptors (NLRs). Surfactant proteins A (SP-A) and D (SP-D) act as pattern recognition receptors and are found in the lung and many other tissues including the ET and the middle ear where they probably function in host defense. Surfactant has a potential for use in the treatment of OM due to surface tension lowering function in the ET, and the possible immune functions of SP-D and SP-A in the middle ear and ET.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 7-8","pages":"213-223"},"PeriodicalIF":3.2,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/23/6a/10.1177_17534259221123309.PMC9900255.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9218295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-01Epub Date: 2022-11-13DOI: 10.1177/17534259221114217
A Otterbeck, P Skorup, K Hanslin, A Larsson, J Stålberg, H Hjelmqvist, M Lipcsey
Ventilator associated pneumonia (VAP) caused by P. aeruginosa is a cause of morbidity and mortality in critically ill patients. The spread of pathogens with anti-microbial resistance mandates the investigation of novel therapies. Specific polyclonal anti-P. aeruginosa IgY-antibodies (Pa-IgY) might be effective for VAP caused by P. aeruginosa. The objective of this study was to investigate if intravenous Pa-IgY decreases the lower airway concentration of P. aeruginosa in VAP. We used a double blind randomized placebo controlled porcine model of VAP caused by P. aeruginosa. Eighteen pigs were randomized to either receive intravenous Pa-IgY or placebo. Repeated registration of physiological parameters and sampling was performed for 27 h. Concentration of P. aeruginosa in BAL-cultures was similar in both groups with 104.97 ± 102.09 CFU/mL in the intervention group vs 104.37 ± 102.62 CFU/mL in the control group at the end of the experiment. The intervention group had higher heart rate, cardiac index, oxygen delivery and arterial oxygen tension/fraction of inspired oxygen-ratio, but lower plasma lactate and blood hemoglobin levels than the control group. In summary, in an anesthetized and mechanically ventilated porcine model of VAP, Pa-IgY at the dose used did not decrease concentrations of P. aeruginosa in the lower airways.
{"title":"Intravenous anti-<i>P. aeruginosa</i> IgY-antibodies do not decrease pulmonary bacterial concentrations in a porcine model of ventilator-associated pneumonia.","authors":"A Otterbeck, P Skorup, K Hanslin, A Larsson, J Stålberg, H Hjelmqvist, M Lipcsey","doi":"10.1177/17534259221114217","DOIUrl":"10.1177/17534259221114217","url":null,"abstract":"<p><p>Ventilator associated pneumonia (VAP) caused by <i>P. aeruginosa</i> is a cause of morbidity and mortality in critically ill patients. The spread of pathogens with anti-microbial resistance mandates the investigation of novel therapies. Specific polyclonal anti-<i>P. aeruginosa</i> IgY-antibodies (<i>Pa-</i>IgY) might be effective for VAP caused by <i>P. aeruginosa.</i> The objective of this study was to investigate if intravenous <i>Pa-</i>IgY decreases the lower airway concentration of <i>P. aeruginosa</i> in VAP. We used a double blind randomized placebo controlled porcine model of VAP caused by <i>P. aeruginosa</i>. Eighteen pigs were randomized to either receive intravenous <i>Pa-</i>IgY or placebo. Repeated registration of physiological parameters and sampling was performed for 27 h. Concentration of <i>P. aeruginosa</i> in BAL-cultures was similar in both groups with 10<sup>4.97</sup> ± 10<sup>2.09</sup> CFU/mL in the intervention group vs 10<sup>4.37</sup> ± 10<sup>2.62</sup> CFU/mL in the control group at the end of the experiment. The intervention group had higher heart rate, cardiac index, oxygen delivery and arterial oxygen tension/fraction of inspired oxygen-ratio, but lower plasma lactate and blood hemoglobin levels than the control group. In summary, in an anesthetized and mechanically ventilated porcine model of VAP, <i>Pa-</i>IgY at the dose used did not decrease concentrations of <i>P. aeruginosa</i> in the lower airways.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 7-8","pages":"224-234"},"PeriodicalIF":3.2,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9900256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9234861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-06-22DOI: 10.1177/17534259221077750
Janet Gallardo-Zapata, Carmen Maldonado-Bernal
At the end of 2019, an outbreak of a severe respiratory disease occurred in Wuhan China, and an increase in cases of unknown pneumonia was alerted. In January 2020, a new coronavirus named SARS-CoV-2 was identified as the cause. The virus spreads primarily through the respiratory tract, and lymphopenia and cytokine storms have been observed in severely ill patients. This suggests the existence of an immune dysregulation as an accompanying event during a serious illness caused by this virus. Natural killer (NK) cells are innate immune responders, critical for virus shedding and immunomodulation. Despite its importance in viral infections, the contribution of NK cells in the fight against SARS-CoV-2 has yet to be deciphered. Different studies in patients with COVID-19 suggest a significant reduction in the number and function of NK cells due to their exhaustion. In this review, we summarize the current understanding of how NK cells respond to SARS-CoV-2 infection.
{"title":"Natural killer cell exhaustion in SARS-CoV-2 infection.","authors":"Janet Gallardo-Zapata, Carmen Maldonado-Bernal","doi":"10.1177/17534259221077750","DOIUrl":"https://doi.org/10.1177/17534259221077750","url":null,"abstract":"<p><p>At the end of 2019, an outbreak of a severe respiratory disease occurred in Wuhan China, and an increase in cases of unknown pneumonia was alerted. In January 2020, a new coronavirus named SARS-CoV-2 was identified as the cause. The virus spreads primarily through the respiratory tract, and lymphopenia and cytokine storms have been observed in severely ill patients. This suggests the existence of an immune dysregulation as an accompanying event during a serious illness caused by this virus. Natural killer (NK) cells are innate immune responders, critical for virus shedding and immunomodulation. Despite its importance in viral infections, the contribution of NK cells in the fight against SARS-CoV-2 has yet to be deciphered. Different studies in patients with COVID-19 suggest a significant reduction in the number and function of NK cells due to their exhaustion. In this review, we summarize the current understanding of how NK cells respond to SARS-CoV-2 infection.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 6","pages":"189-198"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/04/1f/10.1177_17534259221077750.PMC9389049.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40209946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01Epub Date: 2022-07-25DOI: 10.1177/17534259221114219
Lisa-Marie Schünemann, Hans-Joachim Schuberth
Innate immune training is defined as a property of innate immune cells to react stronger to a secondary contact with pathogens. Induction of innate immune training has been reported for a variety of pathogens and selected pattern recognition receptor-ligands, such as β-glucans (βG). We examined whether Saccharomyces cerevisiae cell wall component βG induces training in bovine monocytes in vitro based on a heightened TNF secretion after stimulation by trained monocyte-derived macrophages with Escherichia coli LPS. Sorted CD14-expressing monocytes (classical and intermediate monocytes), as well as single populations of sorted classical, intermediate and non-classical monocytes could not be trained by βG, whereas macrophages derived from plastic-adherent mononuclear cell preparations displayed features of a trained function. The hypothesis, that non-classical monocytes need to be present in a mixed monocyte population in order to be trained by βG could be verified by a successful training of positively sorted whole monocyte populations (CD14CD16/M) containing all three monocyte subpopulations. The trainability depended on conditions favoring M1 polarization of macrophages. Altogether, innate immune training of bovine monocytes seems to depend on the presence of non-classical monocytes. This adds new information to the role of this monocyte subpopulation in the bovine immune system.
{"title":"Non-classical monocytes contribute to innate immune training in cattle.","authors":"Lisa-Marie Schünemann, Hans-Joachim Schuberth","doi":"10.1177/17534259221114219","DOIUrl":"https://doi.org/10.1177/17534259221114219","url":null,"abstract":"<p><p>Innate immune training is defined as a property of innate immune cells to react stronger to a secondary contact with pathogens. Induction of innate immune training has been reported for a variety of pathogens and selected pattern recognition receptor-ligands, such as β-glucans (βG). We examined whether <i>Saccharomyces cerevisiae</i> cell wall component βG induces training in bovine monocytes <i>in vitro</i> based on a heightened TNF secretion after stimulation by trained monocyte-derived macrophages with <i>Escherichia coli</i> LPS. Sorted CD14-expressing monocytes (classical and intermediate monocytes), as well as single populations of sorted classical, intermediate and non-classical monocytes could not be trained by βG, whereas macrophages derived from plastic-adherent mononuclear cell preparations displayed features of a trained function. The hypothesis, that non-classical monocytes need to be present in a mixed monocyte population in order to be trained by βG could be verified by a successful training of positively sorted whole monocyte populations (CD14CD16/M) containing all three monocyte subpopulations. The trainability depended on conditions favoring M1 polarization of macrophages. Altogether, innate immune training of bovine monocytes seems to depend on the presence of non-classical monocytes. This adds new information to the role of this monocyte subpopulation in the bovine immune system.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 6","pages":"199-210"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7d/05/10.1177_17534259221114219.PMC9389050.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40623438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-08-01DOI: 10.1177/17534259221116799
J. Cavaillon
Louis Selim Chedid was born in Cairo (Egypt) in June 1922 anddied inParis inMarch2021at the ageof98.After obtaining his bachelor’s degree in Cairo, he started hismedical studies in Beirut and completed them in Paris, defending his medical thesis on artificial estrogen in 1947. After being trained in Egypt and the United States, he joined the laboratory of Robert Courrier at the College de France (1946). In 1952, he was recruited by the CNRS (National Center for Scientific Research, France). In 1955, he defended his PhD on hormones and infection and started working at the Institut Pasteur (Paris) in the laboratory of Therapeutic Chemistry under André Lamensans.He joined the Institut Pasteur in 1961 andwas promoted to Professor in 1972. In 1973, he became the head of the Experimental Immunotherapy laboratory. In 1986, he moved to the H. Lee Moffit Cancer Center and Research Institute at the Universiy of South Florida, Tampa where he founded a startup working on vaccine adjuvants (VacSyn). Louis Chedid was the co-author of 26 patents. He investigated immune mechanisms with the goal of boosting the defense against infections. Among his main contributions is the identification with Edgar Lederer (1908–1988) of the muramyl dipeptide (MDP), the smallest active part of the peptidoglycan of mycobacteria present in complete Freund adjuvant. He then devoted part of his career to study homologs of MDP and their bioactivities, synthetic vaccines, and adjuvants. He also performed numerous investigations on endotoxins including investigations on enhanced resistance to infection by endotoxins, LPS-induced abortion, production of interleukin-1 and tumor necrosis factor in response to endotoxins, the synergy between MDP and LPS, prevention of endotoxin-induced lethality, the influence of endotoxin on bone marrow cells, endotoxin tolerance, polyclonal activation, LPS-induced radioresistance, localization of injected Cr-labeled LPS, and studies on alkalyl detoxified endotoxins. He offered the basis for an universal anti-endotoxin antibody: “Thereafter, the presence of a few types of “R’ (rough) antibodies or of serum factors reacting with rough antigens have the capability of coping, like masterkeys, with a wide range of infection due to serologically unrelated organisms”. He collaborated with eminent US scientists including JJ Oppenheim, HS Warren, CA Dinarello, SM Wolff, and JM Krueger. With the latter three, he investigated the links between slow wave sleep and IL-1, his most cited paper (462 citations), and addressed the links between sleep and MDP. A Romanian scientist, Constantin Bona (1934–2015) worked for a while in his laboratory on so-called nonspecific immunity before joining the Mount Sinaï Hospital in New York, working on idiotypes and neonatal immunity. They are co-authors of 17 papers including reports on a Nocardia water soluble mitogen. Claude Leclerc started her bright career on vaccines and cancer at Institut Pasteur in his laboratory. Based on an
路易·塞利姆·谢迪德1922年6月出生于埃及开罗,2021年3月在巴黎去世,享年98岁。在开罗获得学士学位后,他在贝鲁特开始医学学习,并在巴黎完成学业,1947年为他关于人工雌激素的医学论文辩护。在埃及和美国接受训练后,他于1946年加入了法兰西学院罗伯特·库里尔的实验室。1952年,他被法国国家科学研究中心录用。1955年,他为自己的激素和感染博士学位辩护,并开始在巴黎巴斯德研究所(Institut Pasteur)的治疗化学实验室工作,导师是安德烈·拉曼桑(andr Lamensans)。1961年加入巴斯德研究所,1972年晋升为教授。1973年,他成为实验免疫疗法实验室的负责人。1986年,他搬到坦帕南佛罗里达大学的H. Lee Moffit癌症中心和研究所,在那里他创立了一家致力于疫苗佐剂(VacSyn)的初创公司。路易斯·切迪德是26项专利的共同作者。他研究了免疫机制,目的是增强对感染的防御。他的主要贡献之一是与Edgar Lederer(1908-1988)鉴定了muramyl二肽(MDP),这是存在于完全弗氏佐剂中的分枝杆菌肽聚糖中最小的活性部分。随后,他将部分职业生涯用于研究MDP的同源物及其生物活性、合成疫苗和佐剂。他还对内毒素进行了大量的研究,包括对内毒素感染的增强抵抗,LPS诱导的流产,内毒素反应中白细胞介素-1和肿瘤坏死因子的产生,MDP和LPS之间的协同作用,内毒素诱导的致死性的预防,内毒素对骨髓细胞的影响,内毒素耐受性,多克隆活化,LPS诱导的辐射抗性,注射cr标记的LPS的定位,以及碱解毒内毒素的研究。他为通用抗内毒素抗体提供了基础:“此后,几种‘R’(粗糙)抗体或与粗糙抗原反应的血清因子的存在,就像万能钥匙一样,具有应对由血清学无关的生物体引起的广泛感染的能力。”他与美国著名科学家合作,包括JJ Oppenheim, HS Warren, CA Dinarello, SM Wolff和JM Krueger。通过后三篇论文,他研究了慢波睡眠和被引用次数最多的论文IL-1(462次)之间的联系,并阐述了睡眠和MDP之间的联系。罗马尼亚科学家康斯坦丁·博纳(Constantin Bona, 1934-2015)在加入纽约Sinaï山医院(Mount Hospital)之前,曾在自己的实验室从事过一段时间的所谓非特异性免疫研究,研究独特型和新生儿免疫。他们是17篇论文的合著者,其中包括关于诺卡菌水溶性丝裂原的报告。克劳德·勒克莱尔在巴斯德研究所的实验室开始了她在疫苗和癌症方面的辉煌事业。基于agn Ullman的想法,她使用百日咳博德泰拉的腺苷酸环化酶毒素将抗原传递到抗原提呈细胞的细胞质中。她的工作是Louis Chedid和Michael Sela (Weizman研究所)开创的合成疫苗工作的延续,使用与白喉毒素片段相对应的肽。1984年,Claude Leclerc研究表明,在抗体的帮助下,细胞内递送MDP可使其佐剂性提高10,000倍。通过Chedid,他们假设MDP受体在细胞内:“MDP的特异性受体存在于巨噬细胞内[…]。为了保持活性,MDP必须在细胞内以足够的浓度存在。之后Dana Philpott和Gabriel Nuñez的团队在2001/ 2002年发现了NOD1和NOD2细胞质模式识别受体。1964年,他获得法国国籍。他获得了生物学会的布沙尔奖(1954年)和伦敦市的克劳德·伯纳德奖
{"title":"ObituaryLouis Selim Chedid, MD PhDIEIIS honorary life member","authors":"J. Cavaillon","doi":"10.1177/17534259221116799","DOIUrl":"https://doi.org/10.1177/17534259221116799","url":null,"abstract":"Louis Selim Chedid was born in Cairo (Egypt) in June 1922 anddied inParis inMarch2021at the ageof98.After obtaining his bachelor’s degree in Cairo, he started hismedical studies in Beirut and completed them in Paris, defending his medical thesis on artificial estrogen in 1947. After being trained in Egypt and the United States, he joined the laboratory of Robert Courrier at the College de France (1946). In 1952, he was recruited by the CNRS (National Center for Scientific Research, France). In 1955, he defended his PhD on hormones and infection and started working at the Institut Pasteur (Paris) in the laboratory of Therapeutic Chemistry under André Lamensans.He joined the Institut Pasteur in 1961 andwas promoted to Professor in 1972. In 1973, he became the head of the Experimental Immunotherapy laboratory. In 1986, he moved to the H. Lee Moffit Cancer Center and Research Institute at the Universiy of South Florida, Tampa where he founded a startup working on vaccine adjuvants (VacSyn). Louis Chedid was the co-author of 26 patents. He investigated immune mechanisms with the goal of boosting the defense against infections. Among his main contributions is the identification with Edgar Lederer (1908–1988) of the muramyl dipeptide (MDP), the smallest active part of the peptidoglycan of mycobacteria present in complete Freund adjuvant. He then devoted part of his career to study homologs of MDP and their bioactivities, synthetic vaccines, and adjuvants. He also performed numerous investigations on endotoxins including investigations on enhanced resistance to infection by endotoxins, LPS-induced abortion, production of interleukin-1 and tumor necrosis factor in response to endotoxins, the synergy between MDP and LPS, prevention of endotoxin-induced lethality, the influence of endotoxin on bone marrow cells, endotoxin tolerance, polyclonal activation, LPS-induced radioresistance, localization of injected Cr-labeled LPS, and studies on alkalyl detoxified endotoxins. He offered the basis for an universal anti-endotoxin antibody: “Thereafter, the presence of a few types of “R’ (rough) antibodies or of serum factors reacting with rough antigens have the capability of coping, like masterkeys, with a wide range of infection due to serologically unrelated organisms”. He collaborated with eminent US scientists including JJ Oppenheim, HS Warren, CA Dinarello, SM Wolff, and JM Krueger. With the latter three, he investigated the links between slow wave sleep and IL-1, his most cited paper (462 citations), and addressed the links between sleep and MDP. A Romanian scientist, Constantin Bona (1934–2015) worked for a while in his laboratory on so-called nonspecific immunity before joining the Mount Sinaï Hospital in New York, working on idiotypes and neonatal immunity. They are co-authors of 17 papers including reports on a Nocardia water soluble mitogen. Claude Leclerc started her bright career on vaccines and cancer at Institut Pasteur in his laboratory. Based on an","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"28 1","pages":"187 - 188"},"PeriodicalIF":3.2,"publicationDate":"2022-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42603474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}