Principles of innate and adaptive immunity
The macrophages and neutrophils of the innate immune system provide a first line of defense against many common microorganisms and are essential for the control of common bacterial infections. However, they cannot always eliminate infectious organisms, and there are some pathogens that they cannot recognize. The lymphocytes of the adaptive immune system have evolved to provide a more versatile means of defense which, in addition, provides increased protection against subsequent reinfection with the same pathogen. The cells of the innate immune system, however, play a crucial part in the initiation and subsequent direction of adaptive immune responses, as well as participating in the removal of pathogens that have been targeted by an adaptive immune response. Moreover, because there is a delay of 4–7 days before the initial adaptive immune response takes effect, the innate immune response has a critical role in controlling infections during this period.
https://www.ncbi.nlm.nih.gov/books/NBK27090/
Principles of innate and adaptive immunity
Re: Principles of innate and adaptive immunity
Biologic Activity of Autologous, Granulocyte-Macrophage Colony-Stimulating Factor Secreting Alveolar Soft-Part Sarcoma and Clear Cell Sarcoma Vaccines.
https://www.ncbi.nlm.nih.gov/m/pubmed/25805798
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https://www.ncbi.nlm.nih.gov/m/pubmed/25805798
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Debbie
Re: Principles of innate and adaptive immunity
This trial was partially sponsored by our iCureASPS society, many of our patients participating in it. The result is inconclusive but the research was used in the future immunotherapy developments.
Olga
Re: Principles of innate and adaptive immunity
Thank you Olga
Do you know if anymore information was found out about the CCS patient and having developed type 1 diabetes ?
“One patient (CCS-8) was diagnosed with type 1 insulin-dependent diabetes one year after completing a course of 12 vaccinations. A cryopreserved serum sample obtained prior to treatment revealed the presence of anti-beta cell antibodies, demonstrating that the autoimmunity predated vaccination. Whether immunization impacted the kinetics of disease development remains unclear, but the diabetes was effectively managed with an insulin pump. No other autoimmune toxicities were observed.”
Looks like they may of had the beginnings of diabetes ?
Anti-beta cell antibodies ?
Do you know if anymore information was found out about the CCS patient and having developed type 1 diabetes ?
“One patient (CCS-8) was diagnosed with type 1 insulin-dependent diabetes one year after completing a course of 12 vaccinations. A cryopreserved serum sample obtained prior to treatment revealed the presence of anti-beta cell antibodies, demonstrating that the autoimmunity predated vaccination. Whether immunization impacted the kinetics of disease development remains unclear, but the diabetes was effectively managed with an insulin pump. No other autoimmune toxicities were observed.”
Looks like they may of had the beginnings of diabetes ?
Anti-beta cell antibodies ?
Debbie
How does friendly fire happen in the pancreas?
How does friendly fire happen in the pancreas?
Date:
October 21, 2016
“In type 1 diabetes, the body attacks its own insulin-producing cells. Scientists at Helmholtz Zentrum München, partner in the German Center for Diabetes Research, and their colleagues at Technical University of Munich have now reported in the journal PNAS about a mechanism used by the immune system to prepare for this attack. They were able to inhibit this process through targeted intervention and are now hoping this will lead to new possibilities for treatment.
Type 1 diabetes is an autoimmune disease in which the body destroys its own beta cells in the pancreas.* Researchers are still seeking to find out what causes this malfunction of the immune system in order to intervene therapeutically in the processes. A team led by Dr. Carolin Daniel, group leader at the Institute of Diabetes Research (IDF) of Helmholtz Zentrum München, has now discovered a further piece in solving this puzzle.
"For the first time, we were able to show that in the affected children an increased number of specific immune cells are found in the blood at the beginning of the autoimmune response," said Daniel. She and her team had previously analyzed blood samples of children in a biobank established by Professor Anette-Gabriele Ziegler, director of the IDF, within the framework of large-scale cohort studies.
According to the authors, these special immune cells are so-called insulin-specific T follicular helper cells (TFH). They appear in the lymph nodes, among other organs, and initiate attacks of the immune system by promoting the production of antibodies by B cells. Now the scientists have found increased frequencies of these cells in samples of children with recent onset of islet cell autoimmunity -- an early stage of type 1 diabetes.”
https://www.sciencedaily.com/releases/2 ... 084517.htm
Date:
October 21, 2016
“In type 1 diabetes, the body attacks its own insulin-producing cells. Scientists at Helmholtz Zentrum München, partner in the German Center for Diabetes Research, and their colleagues at Technical University of Munich have now reported in the journal PNAS about a mechanism used by the immune system to prepare for this attack. They were able to inhibit this process through targeted intervention and are now hoping this will lead to new possibilities for treatment.
Type 1 diabetes is an autoimmune disease in which the body destroys its own beta cells in the pancreas.* Researchers are still seeking to find out what causes this malfunction of the immune system in order to intervene therapeutically in the processes. A team led by Dr. Carolin Daniel, group leader at the Institute of Diabetes Research (IDF) of Helmholtz Zentrum München, has now discovered a further piece in solving this puzzle.
"For the first time, we were able to show that in the affected children an increased number of specific immune cells are found in the blood at the beginning of the autoimmune response," said Daniel. She and her team had previously analyzed blood samples of children in a biobank established by Professor Anette-Gabriele Ziegler, director of the IDF, within the framework of large-scale cohort studies.
According to the authors, these special immune cells are so-called insulin-specific T follicular helper cells (TFH). They appear in the lymph nodes, among other organs, and initiate attacks of the immune system by promoting the production of antibodies by B cells. Now the scientists have found increased frequencies of these cells in samples of children with recent onset of islet cell autoimmunity -- an early stage of type 1 diabetes.”
https://www.sciencedaily.com/releases/2 ... 084517.htm
Debbie
Re: Principles of innate and adaptive immunity
How does friendly fire happen in the pancreas?
“In the search for the causes of the increase in TFH cells during autoimmune activation in children, the scientists discovered a previously unknown signaling pathway. "Our analyses showed that a molecule called miRNA92a** triggers a chain of molecular events, which ultimately leads to the increase in these immune cells," said IDF doctoral student Isabelle Serr, explaining the complex mechanism. "In particular, during this process, miRNA92a interferes with the formation of important signaling proteins such as KLF2 and PTEN."
Friend or foe: the role of microRNA in chemotherapy resistance
Abstract
Chemotherapy has been widely used in treating cancer patients. Despite the tremendous progress in cancer treatment achieved during the last decades, drug resistance still accounts for most of the tumor relapses in chemotherapy-treated patients. Emerging evidence shows that microRNAs play an important role in regulating the drug sensitivity of tumor cells. However, the mechanism of microRNA-mediated drug resistance is not fully understood. Current data suggest that microRNAs can be categorized as oncogenic or tumor-suppressive based on their functions and targets. In tumor cells undergoing drug treatment, microRNAs can function either by decreasing expression of genes associated with multiple drug resistance or by promoting escape from apoptosis and inducing tumor stem cell development. This review aims to provide an updated understanding of the role of microRNAs in regulating chemotherapy resistance and a discussion of potential therapeutic applications.
https://www.nature.com/articles/aps201335
“In the search for the causes of the increase in TFH cells during autoimmune activation in children, the scientists discovered a previously unknown signaling pathway. "Our analyses showed that a molecule called miRNA92a** triggers a chain of molecular events, which ultimately leads to the increase in these immune cells," said IDF doctoral student Isabelle Serr, explaining the complex mechanism. "In particular, during this process, miRNA92a interferes with the formation of important signaling proteins such as KLF2 and PTEN."
Friend or foe: the role of microRNA in chemotherapy resistance
Abstract
Chemotherapy has been widely used in treating cancer patients. Despite the tremendous progress in cancer treatment achieved during the last decades, drug resistance still accounts for most of the tumor relapses in chemotherapy-treated patients. Emerging evidence shows that microRNAs play an important role in regulating the drug sensitivity of tumor cells. However, the mechanism of microRNA-mediated drug resistance is not fully understood. Current data suggest that microRNAs can be categorized as oncogenic or tumor-suppressive based on their functions and targets. In tumor cells undergoing drug treatment, microRNAs can function either by decreasing expression of genes associated with multiple drug resistance or by promoting escape from apoptosis and inducing tumor stem cell development. This review aims to provide an updated understanding of the role of microRNAs in regulating chemotherapy resistance and a discussion of potential therapeutic applications.
https://www.nature.com/articles/aps201335
Debbie
Friend or foe: the role of microRNA in chemotherapy resistance
Friend or foe: the role of microRNA in chemotherapy resistance
Introduction
Chemotherapy, together with surgery and radiotherapy, has been a main approach for cancer treatment. Most chemotherapeutic agents function by interfering with DNA replication and cell mitosis, inhibiting protein synthesis and inducing cell damage. Chemotherapy is often effective in diminishing rapid tumor cell growth as well as minimizing metastatic disease. In recent decades, tremendous efforts have been made to improve the efficacy of anticancer agents. For malignancies such as lymphoma, leukemia and small cell lung cancer, chemotherapy has been used as first-line therapy. As an adjuvant therapy, chemotherapy is widely used to prevent tumor recurrence by eliminating residual lesions. When used alone or combined with radiotherapy, neoadjuvant chemotherapy can even reduce tumor size before surgery, curing otherwise incurable patients. However, the development of drug resistance often results in the failure of chemotherapy, especially in advanced cancer patients. In general, there are two classes of drug resistance: inherent (natural) resistance and acquired resistance. Inherent resistance can be partially overcome by incorporating multiple agents into chemotherapy regimens, while acquired resistance to chemotherapeutic drugs accounts for greater than 90% of unsuccessful treatments in advanced cancer patients1. As a result of drug resistance, tumors often relapse more aggressively and metastasize to distant organs, leading to devastating outcomes. The mechanisms of chemotherapeutic drug resistance still remain largely unknown despite extensive investigation. The response of cancer cells to treatment indicates that chemotherapy resistance could be due to either genetic or epigenetic factors, including (1) overexpression of drug resistance-related proteins, (2) altered drug targets, (3) decreases in drug concentrations, and (4) escape from cell cycle checkpoints. Emerging evidence indicates that tumor angiogenesis and stem cell development are also responsible for chemoresistance.
Introduction
Chemotherapy, together with surgery and radiotherapy, has been a main approach for cancer treatment. Most chemotherapeutic agents function by interfering with DNA replication and cell mitosis, inhibiting protein synthesis and inducing cell damage. Chemotherapy is often effective in diminishing rapid tumor cell growth as well as minimizing metastatic disease. In recent decades, tremendous efforts have been made to improve the efficacy of anticancer agents. For malignancies such as lymphoma, leukemia and small cell lung cancer, chemotherapy has been used as first-line therapy. As an adjuvant therapy, chemotherapy is widely used to prevent tumor recurrence by eliminating residual lesions. When used alone or combined with radiotherapy, neoadjuvant chemotherapy can even reduce tumor size before surgery, curing otherwise incurable patients. However, the development of drug resistance often results in the failure of chemotherapy, especially in advanced cancer patients. In general, there are two classes of drug resistance: inherent (natural) resistance and acquired resistance. Inherent resistance can be partially overcome by incorporating multiple agents into chemotherapy regimens, while acquired resistance to chemotherapeutic drugs accounts for greater than 90% of unsuccessful treatments in advanced cancer patients1. As a result of drug resistance, tumors often relapse more aggressively and metastasize to distant organs, leading to devastating outcomes. The mechanisms of chemotherapeutic drug resistance still remain largely unknown despite extensive investigation. The response of cancer cells to treatment indicates that chemotherapy resistance could be due to either genetic or epigenetic factors, including (1) overexpression of drug resistance-related proteins, (2) altered drug targets, (3) decreases in drug concentrations, and (4) escape from cell cycle checkpoints. Emerging evidence indicates that tumor angiogenesis and stem cell development are also responsible for chemoresistance.
Last edited by D.ap on Sat Jul 11, 2020 2:31 am, edited 1 time in total.
Debbie
Friend or foe: the role of microRNA in chemotherapy resistance
“It is known that cancer consists of a group of genetically heterogenetic cells. Chemotherapeutic drug treatment transforms predominant, fast-dividing cells into drug-resistant ones. These cells are thought to be the cause of subsequent tumor recurrence. During transformation, tumor cells undergo dramatic changes at the genetic and epigenetic level. MicroRNAs (miRNAs) have evolved as a major force in regulating gene expression and the phenotype of tumor cells because of their diverse functions in cell proliferation2,3,4, cell cycle progression5,6,7, survival8,9, invasion10,11,12, cell differentiation13,14, and morphogenesis15. The activities of miRNAs are also regulated by non-coding RNAs. This was initially demonstrated by us using the 3′UTR of versican, which induces organ adhesion by modulating miRNA function16,17. Further studies indicated that a number of 3′UTRs possess the ability to regulate miRNA function18,19,20. In addition, pseudogenes and long non-coding RNAs can modulate miRNA function21,22. This complicated network makes it difficult to understand the intrinsic mechanisms. Hence, there is a pressing need to decipher the molecular mechanism of miRNA-regulated drug resistance and its therapeutic implications. In this review, the role of microRNAs in anticancer drug resistance will be explored in light of current knowledge.”
https://www.nature.com/articles/aps201335
https://www.nature.com/articles/aps201335
Debbie
The innate and adaptive immune systems
The innate and adaptive immune systems
“The immune system fights germs and foreign substances on the skin, in the tissues of the body and in bodily fluids such as blood. The immune system is made up of two parts: the innate, (general) immune system and the adaptive (specialized) immune system. These two systems work closely together and take on different tasks.”
https://www.ncbi.nlm.nih.gov/books/NBK279396/
“The immune system fights germs and foreign substances on the skin, in the tissues of the body and in bodily fluids such as blood. The immune system is made up of two parts: the innate, (general) immune system and the adaptive (specialized) immune system. These two systems work closely together and take on different tasks.”
https://www.ncbi.nlm.nih.gov/books/NBK279396/
Debbie