Pub Date : 2021-01-01DOI: 10.1615/forumimmundisther.2021040911
S. Romero‐Garcia, Ángeles Carlos-Reyes, H. Prado-Garcia
{"title":"A brief review on metabolic evasion mechanisms of tumor cells against T cells","authors":"S. Romero‐Garcia, Ángeles Carlos-Reyes, H. Prado-Garcia","doi":"10.1615/forumimmundisther.2021040911","DOIUrl":"https://doi.org/10.1615/forumimmundisther.2021040911","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/ForumImmunDisTher.2017019469
D Scott Samuels, Leah R N Samuels
Borrelia burgdorferi, the spirochete that causes Lyme disease, exists in an enzootic cycle, alternating between a tick vector and a vertebrate host. To adapt to and survive the environmental changes associated with its enzootic cycle, including nutrient availability, B. burgdorferi uses three different systems to regulate the expression of genes: RpoN-RpoS, histidine kinase (Hk)1/response regulator 1 (Rrp1), and RelBbu. The RpoN-RpoS alternative sigma factor cascade activates genes required for transmission from the tick to the vertebrate, maintenance of the vertebrate infection, and persistence in the tick. RelBbu controls the levels of the alarmones guanosine pentaphosphate and guanosine tetraphosphate, which are necessary for surviving the nutrient-deficient conditions in the midgut of the tick following absorption of the blood meal and the subsequent molt. The Hk1/Rrp1 two-component system produces cyclic dimeric guanosine monophosphate that regulates the genes required for the transitions between the tick and vertebrate as well as protective responses to the blood meal.
{"title":"Gene Regulation During the Enzootic Cycle of the Lyme Disease Spirochete.","authors":"D Scott Samuels, Leah R N Samuels","doi":"10.1615/ForumImmunDisTher.2017019469","DOIUrl":"https://doi.org/10.1615/ForumImmunDisTher.2017019469","url":null,"abstract":"<p><p><i>Borrelia burgdorferi</i>, the spirochete that causes Lyme disease, exists in an enzootic cycle, alternating between a tick vector and a vertebrate host. To adapt to and survive the environmental changes associated with its enzootic cycle, including nutrient availability, <i>B. burgdorferi</i> uses three different systems to regulate the expression of genes: RpoN-RpoS, histidine kinase (Hk)1/response regulator 1 (Rrp1), and Rel<sub>Bbu</sub>. The RpoN-RpoS alternative sigma factor cascade activates genes required for transmission from the tick to the vertebrate, maintenance of the vertebrate infection, and persistence in the tick. Rel<sub>Bbu</sub> controls the levels of the alarmones guanosine pentaphosphate and guanosine tetraphosphate, which are necessary for surviving the nutrient-deficient conditions in the midgut of the tick following absorption of the blood meal and the subsequent molt. The Hk1/Rrp1 two-component system produces cyclic dimeric guanosine monophosphate that regulates the genes required for the transitions between the tick and vertebrate as well as protective responses to the blood meal.</p>","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 3-4","pages":"205-212"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5985821/pdf/nihms970534.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36199570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/ForumImmunDisTher.2016017095
Nabil Aziz, Benjamin Bonavida
During the last decade, probiotics have been established to be important mediators of host immunity. Their effects on both innate and adaptive immunity have been documented in the literature. Although several reports have correlated different strains of bacteria as probiotics, their effects on immunity vary. Clearly, there is a complex interplay between various constituents of probiotics and the immune response in humans. The role of probiotics on natural killer (NK) cells in the gut has been the subject of a few reports. In this review, we summarize the reported findings on the role of probiotics in the activation of gut-associated NK cells and the response of NK cells to stimuli elicited by probiotics and their microenvironment. The effects of probiotics on the activation of NK cells and their secretion of immune factors (e.g., interferon-γ, tumor necrosis factor-α, interleukin-2, etc.) are discussed in regard to their clinical significance in various diseases. Current investigations are being pursued, in particular, on the role of probiotics-activated NK cells in promoting the adaptive immune response against pathogens.
{"title":"Activation of Natural Killer Cells by Probiotics.","authors":"Nabil Aziz, Benjamin Bonavida","doi":"10.1615/ForumImmunDisTher.2016017095","DOIUrl":"https://doi.org/10.1615/ForumImmunDisTher.2016017095","url":null,"abstract":"<p><p>During the last decade, probiotics have been established to be important mediators of host immunity. Their effects on both innate and adaptive immunity have been documented in the literature. Although several reports have correlated different strains of bacteria as probiotics, their effects on immunity vary. Clearly, there is a complex interplay between various constituents of probiotics and the immune response in humans. The role of probiotics on natural killer (NK) cells in the gut has been the subject of a few reports. In this review, we summarize the reported findings on the role of probiotics in the activation of gut-associated NK cells and the response of NK cells to stimuli elicited by probiotics and their microenvironment. The effects of probiotics on the activation of NK cells and their secretion of immune factors (e.g., interferon-γ, tumor necrosis factor-α, interleukin-2, etc.) are discussed in regard to their clinical significance in various diseases. Current investigations are being pursued, in particular, on the role of probiotics-activated NK cells in promoting the adaptive immune response against pathogens.</p>","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1-2","pages":"41-55"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1615/ForumImmunDisTher.2016017095","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35090003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2017020223
N. Charon
{"title":"The University of California at Los Angeles and James Miller: A Powerhouse","authors":"N. Charon","doi":"10.1615/FORUMIMMUNDISTHER.2017020223","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2017020223","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"161"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2016018247
W. Ai
{"title":"Role of Immune-Cell−Expressing Kruppel-Like Factor 4 in Cancer Development","authors":"W. Ai","doi":"10.1615/FORUMIMMUNDISTHER.2016018247","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2016018247","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"61-75"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2016018570
A. Goyal, T. Garg, Goutam Rath
{"title":"Probiotics in Human Health","authors":"A. Goyal, T. Garg, Goutam Rath","doi":"10.1615/FORUMIMMUNDISTHER.2016018570","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2016018570","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"17-31"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1615/FORUMIMMUNDISTHER.2016018570","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2017020106
B. Bonavida
{"title":"A Tribute to James N. Miller: Colleague−Friend− Mentor","authors":"B. Bonavida","doi":"10.1615/FORUMIMMUNDISTHER.2017020106","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2017020106","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"165"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2017020474
L. Bockenstedt
{"title":"A Tribute to James N. Miller","authors":"L. Bockenstedt","doi":"10.1615/FORUMIMMUNDISTHER.2017020474","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2017020474","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"163-164"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440796","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/FORUMIMMUNDISTHER.2017020504
J. Nally
{"title":"Dr. James N. Miller: Virtuoso of All Spirochetes","authors":"J. Nally","doi":"10.1615/FORUMIMMUNDISTHER.2017020504","DOIUrl":"https://doi.org/10.1615/FORUMIMMUNDISTHER.2017020504","url":null,"abstract":"","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 1","pages":"159"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67440813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1615/ForumImmunDisTher.2017020293
David A Haake
The immune response is a cornerstone in the body's struggle against microbial pathogens. In ways that we do not yet completely understand, the mammalian immune response has evolved to identify proteins of pathogens that are either important virulence factors or key immunoprotective targets. Professor James N. Miller suggested that one way to discover such proteins is to harness the power of the immune system in the laboratory.This general concept, referred to here as the Miller Hypothesis, took several different manifestations in the discovery of some of the best known and widely studied leptospiral proteins: The porin OmpL1 was identified by surface immunoprecipitation, leptospiral immunoglobulin-like proteins were uncovered by screening a genomic library with sera from leptospirosis patients, and the major outer-membrane lipoprotein LipL32 was recognized through immunoblot studies. Such approaches will continue to bear fruit for both the leptospiral research field and research on other invasive pathogens.
免疫反应是人体对抗微生物病原体的基石。哺乳动物的免疫反应已经进化到可以识别病原体的蛋白质，这些蛋白质要么是重要的毒力因子，要么是关键的免疫保护靶点。詹姆斯·n·米勒(James N. Miller)教授建议，发现这种蛋白质的一种方法是在实验室中利用免疫系统的力量。这一普遍概念，在这里被称为米勒假说，在发现一些最著名和被广泛研究的钩端螺旋体蛋白时表现出了几种不同的表现:通过表面免疫沉淀鉴定了孔蛋白OmpL1，通过筛选钩端螺旋体患者血清的基因组文库发现了钩端螺旋体免疫球蛋白样蛋白，通过免疫印迹研究识别了主要的外膜脂蛋白LipL32。这种方法将继续在钩端螺旋体研究领域和其他侵入性病原体的研究中取得成果。
{"title":"The Miller Hypothesis.","authors":"David A Haake","doi":"10.1615/ForumImmunDisTher.2017020293","DOIUrl":"https://doi.org/10.1615/ForumImmunDisTher.2017020293","url":null,"abstract":"<p><p>The immune response is a cornerstone in the body's struggle against microbial pathogens. In ways that we do not yet completely understand, the mammalian immune response has evolved to identify proteins of pathogens that are either important virulence factors or key immunoprotective targets. Professor James N. Miller suggested that one way to discover such proteins is to harness the power of the immune system in the laboratory.This general concept, referred to here as the Miller Hypothesis, took several different manifestations in the discovery of some of the best known and widely studied leptospiral proteins: The porin OmpL1 was identified by surface immunoprecipitation, leptospiral immunoglobulin-like proteins were uncovered by screening a genomic library with sera from leptospirosis patients, and the major outer-membrane lipoprotein LipL32 was recognized through immunoblot studies. Such approaches will continue to bear fruit for both the leptospiral research field and research on other invasive pathogens.</p>","PeriodicalId":89370,"journal":{"name":"Forum on immunopathological diseases and therapeutics","volume":"7 3-4","pages":"167-174"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1615/ForumImmunDisTher.2017020293","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36913455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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