Academic literature on the topic 'Plasma proteins; Humoral immune system'
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Journal articles on the topic "Plasma proteins; Humoral immune system"
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Trezise, Stephanie, Alexander Karnowski, Pasquale Fedele, Sridurga Mithraprabhu, Yang Liao, Kathy D’Costa, Andrew Kueh, et al. "Mining the Plasma Cell Transcriptome for Novel Cell Surface Proteins." International Journal of Molecular Sciences 19, no. 8 (July 24, 2018): 2161. http://dx.doi.org/10.3390/ijms19082161.
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Antibody Secreting Cells (ASCs) are a fundamental component of humoral immunity, however, deregulated or excessive antibody production contributes to the pathology of autoimmune diseases, while transformation of ASCs results in the malignancy Multiple Myeloma (MM). Despite substantial recent improvements in treating these conditions, there is as yet no widely used ASC-specific therapeutic approach, highlighting a critical need to identify novel methods of targeting normal and malignant ASCs. Surface molecules specifically expressed by the target cell population represent ideal candidates for a monoclonal antibody-based therapy. By interrogating the ASC gene signature that we previously defined we identified three surface proteins, Plpp5, Clptm1l and Itm2c, which represent potential targets for novel MM treatments. Plpp5, Clptm1l and Itm2c are highly and selectively expressed by mouse and human ASCs as well as MM cells. To investigate the function of these proteins within the humoral immune system we have generated three novel mouse strains, each carrying a loss-of-function mutation in either Plpp5, Clptm1l or Itm2c. Through analysis of these novel strains, we have shown that Plpp5, Clptm1l and Itm2c are dispensable for the development, maturation and differentiation of B-lymphocytes, and for the production of antibodies by ASCs. As adult mice lacking either protein showed no apparent disease phenotypes, it is likely that targeting these molecules on ASCs will have minimal on-target adverse effects.
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Zhang, Yi, Jun Li, Ya-Min Zhang, Xiao-Ming Zhang, and Juan Tao. "Effect of TACI Signaling on Humoral Immunity and Autoimmune Diseases." Journal of Immunology Research 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/247426.
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Transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) is one of the receptors of B cell activating factor of the tumor necrosis factor family (BAFF) and a proliferation-inducing ligand (APRIL). TACI is a regulator in the immune responses. TACI inhibits B cell expansion and promotes the differentiation and survival of plasma cells. The mechanisms underlying these effects probably involve changed expressions of some crucial molecules, such as B lymphocyte induced maturation protein-1 (Blimp-1) and inducible T-cell costimulator ligand (ICOSL) in B cells and/or plasma cells. However, abnormal TACI signaling may relate to autoimmune disorders. Common variable immune deficiency (CVID) patients with heterozygous mutations inTACIalleles increase susceptibility to autoimmune diseases.Taci−/−mice and BAFF transgenic mice both develop signs of human SLE. These findings that indicate inappropriate levels of TACI signaling may disrupt immune system balance, thereby promoting the development of autoimmune diseases. In this review, we summarize the basic characteristics of the TACI ligands BAFF and APRIL, and detail the research findings on the role of TACI in humoral immunity. We also discuss the possible mechanisms underlying the susceptibility of CVID patients withTACImutations to autoimmune diseases and the role of TACI in the pathogenesis of SLE.
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Nieman, David, Arnoud Groen, Artyom Pugachev, Andrew Simonson, Kristine Polley, Karma James, Bassem El-Khodor, Saradhadevi Varadharaj, and Claudia Hernández-Armenta. "Blood Proteomics-Based Detection of Upregulated Lipid Metabolism and Immune Dysfunction in an Elite Adventure Athlete Trekking Across Antarctica." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1760. http://dx.doi.org/10.1093/cdn/nzaa066_015.
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Abstract Objectives Proteomics when combined with psychological, nutrition, and performance measures may serve as a useful monitoring system for immune dysfunction, training distress, and exercise-induced muscle damage and exhaustion in athletes. Global proteomics monitoring of an elite adventure athlete (age 33 years) was conducted over a 28-week period that culminated in the successful, unassisted 2-month trek across Antarctica (1500 km). Methods Training distress was monitored weekly using the 19-item, validated Training Distress Scale (TDS). Weekly dried blood spot (DBS) specimens were collected via fingerprick blood drops onto standard blood spot cards. DBS proteins were measured with nano-electrospray ionization liquid chromatography tandem mass spectrometry (nanoLC-MS/MS) in data-independent acquisition (DIA) mode, and 712 proteins were identified and quantified. Results The participant experienced a decrease of 11.4 kg in body mass during the Antarctica trek. The 28-week period was divided into time segments based on TDS scores, and a contrast analysis between weeks 5–8 (low TDS) and weeks 20–23 (high TDS, last month of Antarctica trek) showed that 31 proteins (n = 20 immune related, n = 14 nutrition related with n = 8 in dual roles) were upregulated and 35 (n = 17 immune related) were downregulated. Protein-protein interaction (PPI) networks and gene ontology (GO) biological process analysis supported an increase in plasma lipoprotein particle remodeling, regulation of lipid transport, retinoid metabolic process, and vitamin transport due to high energy intake (7048 kcal/d). PPI networks also supported a dichotomous immune response. GO terms for the upregulated immune proteins showed an increase in regulation of the immune system process, especially inflammation, complement activation, and leukocyte mediated immunity. GO terms for the downregulated immune-related proteins indicated a decrease in several aspects of the overall immune system process including neutrophil degranulation and the antimicrobial humoral response. Conclusions These proteomics data support a dysfunctional immune response in an elite adventure athlete during a sustained period of mental and physical distress, high energy intake, and significant loss of body mass while trekking solo across Antarctica. Funding Sources Standard Process, Inc., Palmyra, WI.
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Tao, Yu, Gaojian Li, Wenqian Zheng, Jianhong Shu, Jian Chen, Fang Yang, Yuehong Wu, and Yulong He. "Development of a Combined Genetic Engineering Vaccine for Porcine Circovirus Type 2 and Mycoplasma Hyopneumoniae by a Baculovirus Expression System." International Journal of Molecular Sciences 20, no. 18 (September 9, 2019): 4425. http://dx.doi.org/10.3390/ijms20184425.
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Mycoplasma hyopneumoniae (Mhp) and porcine circovirus type 2 (PCV2) are the main pathogens for mycoplasmal pneumonia of swine (MPS) and post-weaning multisystemic wasting syndrome (PMWS), respectively. Infection by these pathogens often happens together and causes great economic losses. In this study, a kind of recombinant baculovirus that can display P97R1P46P42 chimeric protein of Mhp and the capsid (Cap) protein of PCV2 was developed, and the protein location was identified. Another recombinant baculovirus was constructed without tag proteins (EGFP, mCherry) and was used to evaluate the immune effect in experiments with BALB/c mice and domestic piglets. Antigen proteins P97R1P46P42 and Cap were expressed successfully; both were anchored on the plasma membrane of cells and the viral envelope. It should be emphasized that in piglet immunization, the recombinant baculovirus vaccine achieved similar immunological effects as the mixed commercial vaccine. Both the piglet and mouse experiments showed that the recombinant baculovirus was able to induce humoral and cellular responses effectively. The results of this study indicate that this recombinant baculovirus is a potential candidate for the further development of more effective combined genetic engineering vaccines against MPS and PMWS. This experiment also provides ideas for vaccine development for other concomitant diseases using the baculovirus expression system.
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Zhong, Xiaofen, Zufeng Guo, Huanghao Yang, Lisheng Peng, Yong Xie, Tin-Yau Wong, Sik-To Lai, and Zhihong Guo. "Amino terminus of the SARS coronavirus protein 3a elicits strong, potentially protective humoral responses in infected patients." Journal of General Virology 87, no. 2 (February 1, 2006): 369–73. http://dx.doi.org/10.1099/vir.0.81078-0.
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The 3a protein of severe acute respiratory syndrome (SARS)-associated coronavirus is expressed and transported to the plasma membrane in tissue cells of infected patients. Its short N-terminal ectodomain was found to elicit strong humoral responses in half of the patients who had recovered from SARS. The ectodomain-specific antibodies from the convalescent-phase plasma readily recognized and induced destruction of 3a-expressing cells in the presence of the human complement system, demonstrating their potential ability to provide immune protection by recognizing and eliminating SARS coronavirus-infected cells that express the target protein. In addition, when coupled to a carrier protein, the ectodomain peptide elicited 3a-specific antibodies in mice and rabbit at high titres. These results showed that the N terminus of the 3a protein is highly immunogenic and elicits potentially protective humoral responses in infected patients. Therefore, the short extracellular domain may be a valuable immunogen in the development of a vaccine for infectious SARS.
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Mahmoud, A. M. A., E. J. De Luna-Santillana, X. Guo, and Mario A. Rodríguez-Pérez. "Parasitism by Cotesia flavipes alters the haemocyte population and phenoloxidase activity of the sugarcane borer, Diatraea saccharalis." Canadian Entomologist 144, no. 4 (May 18, 2012): 599–608. http://dx.doi.org/10.4039/tce.2012.41.
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AbstractParasitism of Diatraea saccharalis (Fabricius) (Lepidoptera: Crambidae) larvae by Cotesia flavipes Cameron (Hymenoptera: Braconidae) or injection of C. flavipes polydnavirus causes numerous alterations in host physiology including developmental arrest, abrogation of host immunity, and biochemical changes in proteins, carbohydrates, glycogen, and lipids. This study focused on changes in haemocyte composition occurring in the cellular immune system of parasitised D. saccharalis larvae. We also analysed the effects of parasitisation by C. flavipes on humoral immunity in terms of phenoloxidase (PO) activity in the host. In nonparasitised D. saccharalis larvae, granular cells represented the main haemocyte type (39%) and plasmatocytes were also present at around 35% among the total haemocytes. The percentages of these two major haemocytes decreased significantly in parasitised larvae after 6 days of parasitoid oviposition and the total haemocyte counts exhibited a significant reduction in parasitised larvae 3 and 6 days following parasitisation. The parasitised larvae also showed a significant decrease in humoral immune capacity as evidenced by reduction of PO activity. Moreover, the plasma had more PO activity than the haemocytes and the parasitised larvae showed less PO activity than the control larvae. This research demonstrates that the parasitism of C. flavipes adversely affects the total haemocyte populations and PO activity of D. saccharalis larvae, which would contribute to host immunosuppression.
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Matsumoto, A. K., J. Kopicky-Burd, R. H. Carter, D. A. Tuveson, T. F. Tedder, and D. T. Fearon. "Intersection of the complement and immune systems: a signal transduction complex of the B lymphocyte-containing complement receptor type 2 and CD19." Journal of Experimental Medicine 173, no. 1 (January 1, 1991): 55–64. http://dx.doi.org/10.1084/jem.173.1.55.
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The complement system augments the humoral immune response, possibly by a mechanism that involves the B lymphocyte membrane receptor, CR2, which binds the C3dg fragment of C3 and triggers several B cell responses in vitro. The present study demonstrates that CR2 associates with a complex of membrane proteins that may mediate signal transduction by ligated CR2. Monoclonal antibodies to CR2 immunoprecipitated from digitonin lysates of Raji B lymphoblastoid cells a membrane complex containing CR2, approximately equimolar amounts of CD19, which is a member of the immunoglobulin superfamily, and three unidentified components: p130, p50, and p20. The complex, which was immunoprecipitated also with anti-CD19, could be dissociated by Nonidet P-40, accounting for its absence in previous studies of CR2. Expression of recombinant CR2 and CD19 in K562 erythroleukemia cells led to formation of a complex that contained not only these two proteins but also p130, p50, and p20, and another component, p14. These unidentified components of the CR2/CD19 complex coimmunoprecipitated with CD19 and not with CR2 from singly transfected cells, indicating primary association with the former. CD19 replicated the capacity of CR2 to interact synergistically with mIgM for increasing free intracellular Ca2+, suggesting that the complex mediates this function of CR2. Therefore, CR2 associates directly with CD19 to become a ligand-binding subunit of a pre-existing signal transduction complex of the B cell that may be representative of a family of membrane protein complexes. This interaction between the complement and immune systems differs from that between immunoglobulin and Clq by involving membrane rather than plasma proteins, and by having complement involved in the afferent phase of the immune response.
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Rafei, Moutih, Jeremy Hsieh, MengYang Li, and Jacques Galipeau. "Marrow-Derived Mesenchymal Stromal Cells Can Block an Antigen-Driven Humoral Response by Suppressing Plasma Cell Activity Via Production of CCL2." Blood 110, no. 11 (November 16, 2007): 1350. http://dx.doi.org/10.1182/blood.v110.11.1350.1350.
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Abstract Marrow-derived Mesenchymal Stromal Cells (MSCs) have been demonstrated to possess powerful immunomodulatory suppressive properties. In vitro studies by many groups have shown that MSCs can suppress th1 immune responses as exemplified by in vitro blockade of a 2-way mixed lymphocyte reaction (MLR) by an assortment of mechanisms including production of soluble factors such as: nitric oxide, transforming growth factor-β, IGF-1 and hepatocyte growth factor. Lately, interesting studies have also demonstrated the potency of MSCs in modulating humoral immunity by inhibiting B-cell migration, proliferation as well as immunoglobulin secretion in vitro. We here sought to further define the ability of autologous MSCs in modulating an ovalbumin (OVA) antigen-specific humoral response in normal immune competent C57BL/6 mice. Immunologically naïve mice were vaccinated with 50 ug of recombinant chicken ovalbumin protein followed by a boost dose 2 weeks later. All mice developed a robust IgM and IgG anti-OVA antibody response as measured in serial plasma samples over time. Following establishment of anti-OVA humoral immunity, test mice (n=10) were administered 1.5 million autologous MSCs in the peritoneal cavity twice at one month interval. Compared with same-treated controls (n=10), we found that MSC treated mice significantly suppressed anti-OVA IgG titer. This inhibitory effect requires metabolically active MSCs since live MSCs inhibited anti-OVA IgG secretion in ELISPOT assays, whereas paraformaldehyde fixed MSCs had no effect. Interestingly, the addition of MSC conditioned media directly on spleen-derived plasma cells derived form OVA immunized mice inhibited OVA-specific IgG secretion in vitro. A cytokine array screen on MSC secretome identified CCL2 as a possible effector molecule in suppressing plasma cell activity, and we found that anti-CCL2 neutralizing antibodies abolished the suppressive effect of MSCs on plasma cells. In conclusion, we have found that MSCs can suppress a pre-established humoral response to a defined antigen in vivo. This effect is contact independent, and requires metabolically active MSCs. MSC-derived CCL2 appears to be a key suppressor of antigen-specific immunoglobulin in this system.
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González-González, María, José María Sayagués, Luis Muñoz-Bellvís, Carlos Eduardo Pedreira, Marcello L. R. de Campos, Jacinto García, José Antonio Alcázar, et al. "Tracking the Antibody Immunome in Sporadic Colorectal Cancer by Using Antigen Self-Assembled Protein Arrays." Cancers 13, no. 11 (May 31, 2021): 2718. http://dx.doi.org/10.3390/cancers13112718.
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Sporadic Colorectal Cancer (sCRC) is the third leading cause of cancer death in the Western world, and the sCRC patients presenting with synchronic metastasis have the poorest prognosis. Genetic alterations accumulated in sCRC tumor cells translate into mutated proteins and/or abnormal protein expression levels, which contribute to the development of sCRC. Then, the tumor-associated proteins (TAAs) might induce the production of auto-antibodies (aAb) via humoral immune response. Here, Nucleic Acid Programmable Protein Arrays (NAPPArray) are employed to identify aAb in plasma samples from a set of 50 sCRC patients compared to seven healthy donors. Our goal was to establish a systematic workflow based on NAPPArray to define differential aAb profiles between healthy individuals and sCRC patients as well as between non-metastatic (n = 38) and metastatic (n = 12) sCRC, in order to gain insight into the role of the humoral immune system in controlling the development and progression of sCRC. Our results showed aAb profile based on 141 TAA including TAAs associated with biological cellular processes altered in genesis and progress of sCRC (e.g., FSCN1, VTI2 and RPS28) that discriminated healthy donors vs. sCRC patients. In addition, the potential capacity of discrimination (between non-metastatic vs. metastatic sCRC) of 7 TAAs (USP5, ML4, MARCKSL1, CKMT1B, HMOX2, VTI2, TP53) have been analyzed individually in an independent cohort of sCRC patients, where two of them (VTI2 and TP53) were validated (AUC ~75%). In turn, these findings provided novel insights into the immunome of sCRC, in combination with transcriptomics profiles and protein antigenicity characterizations, wich might lead to the identification of novel sCRC biomarkers that might be of clinical utility for early diagnosis of the tumor. These results explore the immunomic analysis as potent source for biomarkers with diagnostic and prognostic value in CRC. Additional prospective studies in larger series of patients are required to confirm the clinical utility of these novel sCRC immunomic biomarkers.
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Sikora, Marta, Ewa Bretes, Joanna Perła-Kaján, Izabela Lewandowska, Łukasz Marczak, and Hieronim Jakubowski. "Genetic Attenuation of Paraoxonase 1 Activity Induces Proatherogenic Changes in Plasma Proteomes of Mice and Humans." Antioxidants 9, no. 12 (November 28, 2020): 1198. http://dx.doi.org/10.3390/antiox9121198.
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High-density lipoprotein (HDL), in addition to promoting reverse cholesterol transport, possesses anti-inflammatory, antioxidative, and antithrombotic activities. Paraoxonase 1 (PON1), carried on HDL in the blood, can contribute to these antiatherogenic activities. The PON1-Q192R polymorphism involves a change from glutamine (Q variant) to arginine (R variant) at position 192 of the PON1 protein and affects its enzymatic activity. The molecular basis of PON1 association with cardiovascular and neurological diseases is not fully understood. To get insight into the function of PON1 in human disease, we examined how genetic attenuation of PON1 levels/activity affect plasma proteomes of mice and humans. Healthy participants (48.9 years old, 50% women) were randomly recruited from the Poznań population. Four-month-old Pon1−/− (n = 17) and Pon1+/+ (n = 8) mice (50% female) were used in these experiments. Plasma proteomes were analyzed using label-free mass spectrometry. Bioinformatics analysis was carried out using the Ingenuity Pathway Analysis (IPA) resources. PON1-Q192R polymorphism and Pon1−/− genotype induced similar changes in plasma proteomes of humans and mice, respectively. The top molecular network, identified by IPA, affected by these changes involved proteins participating in lipoprotein metabolism. Other PON1 genotype-dependent proteomic changes affect different biological networks in humans and mice: “cardiovascular, neurological disease, organismal injury/abnormalities” in PON1-192QQ humans and “humoral immune response, inflammatory response, protein synthesis” and “cell-to-cell signaling/interaction, hematological system development/function, immune cell trafficking” in Pon1−/− mice. Our findings suggest that PON1 interacts with molecular pathways involved in lipoprotein metabolism, acute/inflammatory response, and complement/blood coagulation that are essential for blood homeostasis. Modulation of those interactions by the PON1 genotype can account for its association with cardiovascular and neurological diseases.
Dissertations / Theses on the topic "Plasma proteins; Humoral immune system"
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Lim, Boon-Leong. "Cloning and expression of a C1q-binding protein and two of the collections (Collectin-43 and lung surfactant protein D)." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.239328.
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Maung, Nang H. "Intranasal Colonization by Streptococcus Pneumoniae Induces Immunological Protection from Pulmonary and Systemic Infection: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/570.
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Given that Streptococcus pneumoniae can cause life-threatening pulmonary and systemic infection, an apparent paradox is that the bacterium resides, usually harmlessly, in the nasopharynx of many people. Humoral immunity is thought to be the primary defense against serious pneumococcal infection, and we hypothesized that nasopharyngeal colonization of mice results in the generation of an antibody response that provides long-term protection against lung infection. We found that survival of of C57L/6 mice after intranasal inoculation with wild-type serotype 4 strain TIGR4 pneumococci required B cells but not T cells, suggesting that nasopharyngeal colonization elicited a protective humoral immune response. In fact, intranasal inoculation resulted in detectable pneumococcal-specific antibody responses, and protected mice against a subsequent high-dose S. pneumoniae pulmonary challenge. B cells were required for this response, and transfer of immune sera from i.n. colonized mice, or monoclonal antibodies against phosphorylcholine, a common surface antigen of S. pneumoniae, was sufficient to confer protection. IgA, which is thought to participate in mucosal immunity, contributed to but was not absolutely required for protection from pulmonary challenge. Protection induced by i.n. colonization lasted at least ten weeks. Although it was partially dependent on T cells, depletion of CD4+ T cells at the time of challenge did not alter protection, suggesting that T cells did not provide essential help in activation of conventional memory cells. Peritoneal B1b cells and radiation-resistant, long-lived antibody secreting cells have previously been shown to secrete anti-pneumococcal antibodies and mediate protection against systemic infection following immunization with killed bacteria or capsular polysaccharide [1, 2]. We found that peritoneal cells were not sufficient for colonization-induced protection, but sub-lethally irradiated mice largely survived pulmonary challenge. Thus, our results are consistent with the hypothesis that nasopharyngeal colonization, a common occurrence in humans, is capable of eliciting extended protection against invasive pneumococcal disease by generating long-lived antibody-secreting cells.
Books on the topic "Plasma proteins; Humoral immune system"
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Allen, Geoffrey. Proteins: Major Non-Immune System Proteins of Blood Plasma (Proteins). JAI Press, 1997.
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Tim, Manser, ed. Specialization and complementation of humoral immune responses to infection. Berlin: Springer, 2007.
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E, Sim, ed. Humoral factors. Oxford: IRL Press at Oxford University Press, 1993.
Find full textBook chapters on the topic "Plasma proteins; Humoral immune system"
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Dwenger, A., G. Regel, G. Schweitzer, G. Röllig, and J. Lindena. "Nonspecific Immune System, Plasma Proteins and Characteristics of the Erythrocyte Insulin Receptor." In Adult Respiratory Distress Syndrome, 91–127. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84098-2_12.
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Botto, Marina, and Matthew C. Pickering. "The complement system." In Oxford Textbook of Medicine, edited by John D. Firth, Christopher P. Conlon, and Timothy M. Cox, 315–24. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0039.
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The complement system, consisting of soluble and membrane-bound proteins, is a major effector mechanism of host defence against infection and inflammatory responses. It has an important role in the removal of immune complexes and dying cells, and also modulates humoral and cell-mediated immune responses. Complement activation occurs through three pathways, each generating enzyme complexes, termed C3 convertases. These cleave native C3 to form C3b and C3a. C3b can covalently attach to surfaces (e.g. pathogen surfaces) where it triggers biological responses following interaction with membrane-bound receptors and can also trigger cleavage of native C5 to C5b and C5a. C5b triggers the formation of the membrane attack complex, which disrupts target cell membrane integrity and may result in cell lysis.
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Lambourne, Jonathan, and Ruaridh Buchanan. "Basic Immunology." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0012.
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There are four major components of the immune system. These include: 1. mechanical barriers to pathogen entry. 2. the innate immune system. 3. the adaptive immune system. 4. the lymphoid organs. Mechanical barriers include skin and mucous membranes and tight junctions between epithelial cells prevent pathogen entry. Breaches can be iatrogenic, for example, IV lines, surgical wounds, and mucositis, and are a large source of healthcare- associated infections. The innate immune system provides the first internal line of defence, as well as initiating and shaping the adaptive immune response. The innate system comprises a range of responses: phagocytosis by neutrophils and macrophages (guided in part by the adaptive immune system), the complement cascade, and the release of antimicrobial peptides by epithelial cells (e.g. defensins, cathelicidin). The adaptive immune system includes both humoral (antibody- mediated) and cell-mediated responses. It is capable of greater diversity and specificity than the innate immune system, and can develop memory to pathogens and provide increased protection on re-exposure. Immune cells are divided into myeloid cells (neutrophils, eosinophils, basophils, mast cells, and monocytes/macrophages) and lymphoid cells (B, T, and NK cells). These all originate in the bone marrow from pluripotent haematopoietic stem cells. The lymphoid organs include the spleen, the lymph nodes, and mucosal-associated lymphoid tissues—which respond to antigens in the blood, tissues, and epithelial surfaces respectively. The three main ‘professional’ phagocytes are macrophages, dendritic cells, and neutrophils. They are similar with respect to how they recognize pathogens, but differ in their principal location and effector functions. Phagocytes express an array of Pattern Recognition Receptors (PRRs) e.g. Toll-like receptors and lectins (proteins that bind carbohydrates). PRRs recognize Pathogen- Associated Molecular Patterns (PAMPs)— elements which are conserved across species, such as cell-surface glycoproteins and nucleic acid sequences. Though limited in number, PRRs have evolved to recognize a huge array of pathogens. Binding of PRRs to PAMPs enhances phagocytosis. Macrophages are tissue-resident phagocytes, initiating and co-ordinating the local immune response. The cytokines and chemokines they produce cause vasodilation and alter the expression of endothelial cell adhesion factors, recruiting circulating immune cells.