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Journal articles on the topic 'Immune response'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 November 2024

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1

A, Kavitha, Priavadhana Rajan Prasaad, Bheema Rao G, and Hemalatha Ganapathy. "Immune Response in Tuberculosis - CD4/CD68 Epitope Mapping." Annals of Pathology and Laboratory Medicine 5, no. 9 (September 14, 2018): A759–763. http://dx.doi.org/10.21276/apalm.1960.

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2

Pleskanovskaya, S. A. "ADАPTIVE TRANSFER OF THE IMMUNE RESPONSE – NEW APPROACHES." European Journal of Natural History, no. 6 2020 (2020): 11–16. http://dx.doi.org/10.17513/ejnh.34134.

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3

GC, Velasquez Serra. "Monitoring of Immune Response Following Covid-19 Vaccination." Virology & Immunology Journal 7, no. 1 (January 4, 2023): 1–9. http://dx.doi.org/10.23880/vij-16000311.

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Introduction: SARS-CoV-2 is an infectious, viral, and contagious disease in which most patients present a mild respiratory condition whose recovery is autonomous and guided by the immune system itself. Objectives: The objectives of this research were to evaluate the immune system, the vaccination doses administered to the inhabitants of the parish of El Recreo, located in the Duran Canton of the Province of Guayas (Ecuador), according to age groups and gender, the vaccination coverage and the incidence of new diseases in the population under study. Material and Methods: This was a descriptive, non-experimental, prospective, cross-sectional, field study. It was carried out during the period from November 2021 to March 2022, during the pandemic of the "Omicron" variant. Results: the predominant age group corresponded to the range of 50-59 years (26.83% and 42; 29.79%) for both genders. We found (90.10%) of the population vaccinated. Another group (3.31%) did not receive the biologic and (6.59%) indicated that they were reluctant to receive the product. The second dose was administered to (83.5%) people in the community, while (14.28%) indicated having received the third dose. (3.04%) became ill after receiving the first doses; (2.63%) the second doses and none of those who received the third doses. It is necessary to alert the population of the need to benefit from the application of the vaccine since it seems to confer a certain degree of protection to the inhabitants and thus, the viral spread, hospitalization and death.

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4

Batchelor, J. R. "Immune response." Nature 337, no. 6204 (January 1989): 220. http://dx.doi.org/10.1038/337220a0.

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5

Malinova, Dessi. "Immune response." Opticon1826 7, no. 12 (April 30, 2012): 22. http://dx.doi.org/10.5334/opt.121214.

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6

Pearson, Steven D. "Immune Response." JAMA: The Journal of the American Medical Association 256, no. 22 (December 12, 1986): 3088. http://dx.doi.org/10.1001/jama.1986.03380220054009.

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7

Jamieson, Amanda Mercedes, Meredith Crane, Yun Xu, and Kayla Lee. "Immune triage: prioritization of host immune responses." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 197.20. http://dx.doi.org/10.4049/jimmunol.196.supp.197.20.

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Abstract The immune response is important in many functions, including host defense against pathogens, wound healing, development, response to cancer, and maintenance of homeostatic physiological responses. We are interested in the concept of immune triage, in that a given host must be able to deal effectively with multiple insults, and at times prioritize immune responses. It is important for the overall health status of the host that the immune system responds effectively to protect essential organs. We have developed several mouse models, focusing on the lung immune response, that allow us to examine different aspects of immune triage. The lung is an essential and delicate organ and thus pulmonary immune responses must be tightly regulated. We have determined that lung infection with influenza A virus (IAV) alters the response to bacterial lung infections. Depending on the bacterial infection, previous infection with IAV can suppress or augment the immune response to bacteria. We have also determined that pulmonary infection with IAV alters many aspects of the systemic immune response. There is a global suppression to systemic bacterial infection, and a decrease in the wound healing response. Our data indicate that the immune system prioritizes lung infections over many other responses. This is most likely due to the importance of the lung in host survival. We have established several regulatory mechanisms by which this immune triage occurs. By understanding how the immune system responds to multiple insults we can improve our understanding of the immune network on a global level.

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8

Kannan, Rajni, Kathleen Madden, and Stephanie Andrews. "Primer on Immuno-Oncology and Immune Response." Clinical Journal of Oncology Nursing 18, no. 3 (May 27, 2014): 311–17. http://dx.doi.org/10.1188/14.cjon.311-317.

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9

AK, Vyas. "The Muddle of Immune Response in Coronavirus Disease-19." Open Access Journal of Microbiology & Biotechnology 5, no. 3 (2020): 1–3. http://dx.doi.org/10.23880/oajmb-16000171.

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Coronavirus Disease-19 (COVID19) caused by the enormously spreadable SARS- CoV-2 virus has appeared as a global pandemic and leads to high mortalities. Approximately 31,243,339 people have been infected so far with this disease which has led to the death of more than 965,103patients as of 21st Sept 2020. There are many drug molecules under-trials are in phase I and II. The numerous possible candidates for vaccine development against this infectious virus are also in the pipeline. Although, so far no molecule as a therapeutics or vaccine for prevention has been approved. Recent reports have observed that severely ill patients have a differential immunological profile compared to mild COVID-19 infection. Current studies globally observed that the cytokine storm maybe leads to the severity of COVID19 infection. In this article, our focus is to describe the present knowledge and status of differential immune profile among patients infected with COVID19 infection and their association with disease progression mild to severe.

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10

Joob, Beuy, and Viroj Wiwanitkit. "Neurocysticercosis, immune status and immune response." Arquivos de Neuro-Psiquiatria 70, no. 9 (September 2012): 750. http://dx.doi.org/10.1590/s0004-282x2012000900023.

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11

Eichner, E. Randy. "Immune Response Question." Physician and Sportsmedicine 27, no. 9 (September 1999): 83. http://dx.doi.org/10.3810/psm.1999.09.1005.

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12

Sarfati, Marika, and Guy Delespesse. "Fetal Immune Response." Science 273, no. 5276 (August 9, 1996): 722–23. http://dx.doi.org/10.1126/science.273.5276.722.b.

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13

Sarfati, Marika, and Guy Delespesse. "Fetal Immune Response." Science 273, no. 5276 (August 9, 1996): 722–23. http://dx.doi.org/10.1126/science.273.5276.722-b.

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14

Sarfati, M., and G. Delespesse. "Fetal Immune Response." Science 273, no. 5276 (August 9, 1996): 721d—725. http://dx.doi.org/10.1126/science.273.5276.721d.

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15

Sarfati, M., and G. Delespesse. "Fetal Immune Response." Science 273, no. 5276 (August 9, 1996): 722b—723b. http://dx.doi.org/10.1126/science.273.5276.722b.

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16

Hurtley, S. M. "Immune Response Regulation." Science's STKE 2006, no. 358 (October 17, 2006): tw366. http://dx.doi.org/10.1126/stke.3582006tw366.

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17

De Moreno De Leblanc, A., J. Valdéz, and G. Perdigón. "Inflammatory Immune Response." European Journal of Inflammation 2, no. 1 (January 2004): 21–31. http://dx.doi.org/10.1177/1721727x0400200104.

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18

Mak, Tak W., and Mary E. Saunders. "THE IMMUNE RESPONSE." Shock 27, no. 2 (February 2007): 220–21. http://dx.doi.org/10.1097/01.shk.0000258367.85587.7b.

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19

Baldwin, Cynthia L. "Immune response overview." Veterinary Microbiology 90, no. 1-4 (December 2002): 365–66. http://dx.doi.org/10.1016/s0378-1135(02)00221-3.

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20

Burroughs, N. J., B. M. P. M. Oliveira, A. A. Pinto, and M. Ferreira. "Immune response dynamics." Mathematical and Computer Modelling 53, no. 7-8 (April 2011): 1410–19. http://dx.doi.org/10.1016/j.mcm.2010.02.040.

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21

Phelps, Jerry. "Headliners: Immune Response." Environmental Health Perspectives 111, no. 10 (August 1, 2003): a521. http://dx.doi.org/10.1289/ehp.111-a521.

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22

Lydyard, P. M. "Immune response overview." Current Opinion in Immunology 1, no. 2 (December 1988): 201–2. http://dx.doi.org/10.1016/0952-7915(88)90001-5.

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23

Arthur Blair, Eric. "Immune deficiency derive a favorable response to IVIg in PANDAS." Psychology and Mental Health Care 2, no. 3 (July 6, 2018): 01–03. http://dx.doi.org/10.31579/2637-8892/032.

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For two decades, pediatric autoimmune neuropsychiatric disorder associated with group a beta hemolytic streptococcal infection (PANDAS) has been treated with high-dose intravenous immune globulin (IVIg) therapy based upon the understanding that the disorder is partly due to post-infectious dysimmunity.

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24

Skok, M. V. "Proposals for the ISS: «Immunity» Experiment Immune response in microgravity." Kosmìčna nauka ì tehnologìâ 6, no. 4 (July 30, 2000): 103. http://dx.doi.org/10.15407/knit2000.04.107.

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25

Barton, B. E., and D. A. Levy. "The Immune Response to a Schistosomacide, Amoscanate Ii. Cell-Mediated Immune Responses." Journal of Immunopharmacology 7, no. 3 (January 1985): 373–83. http://dx.doi.org/10.3109/08923978509026482.

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26

Hamadou, Takieddine, Imene Hamadou, Ahmed Menad, Somia Bouameur, and Souad Ameddah. "COVID-19 : histoire, pathogenèse et réponse immunitaire de l'hôte." Batna Journal of Medical Sciences (BJMS) 8, no. 1 (June 4, 2021): 52–58. http://dx.doi.org/10.48087/bjmsra.2021.8110.

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By the end of 2019, pneumonia of unknown etiology occurred in Wuhan, China. Local hospitals started receiving patients presenting symptoms like dry cough, fatigue, and breathing difficulties, most of these patients were linked to the Huanan seafood market, Wuhan, China. The pandemic was afterward confirmed to be associated with a novel coronavirus. The virus spread quickly from Wuhan to other provinces of China, then from china to the rest of the world causing thereby one of the most brutal pandemics in the world’s history. SARS-CoV2 has a long incubation period ranging from 3 to 7 days and can go up to 14 days in some cases which makes the infection difficult to be detected early and subsequently the disease spread harder to be controlled. SARS-CoV-2 is a single-stranded RNA virus with 4 main structural proteins, the spike (S) glycoprotein, the small envelope (E) the glycoprotein, the membrane (M) glycoprotein as well as the nucleocapsid (N) protein. Current knowledge about the virus shows that it uses its spike protein to invade host cells, mainly the alveolar epithelial cells. The the lung is the most targeted organ among many other organs like the heart, small intestine, and kidneys that are vulnerable to SARS-CoV-2 infection. The COVID-19 is known to be mild in most cases, but in some cases, it can be severe or even fatal. In the severe cases, acute respiratory distress syndrome was reported, and the the capability of SARS-CoV-2 to infect many organs can lead to multiorgan failure and death. SARS-CoV-2 invasion induces several immune responses that could be efficient for infection clearance in mild cases, while in severe cases, the immune response dysfunctions can even contribute to the disease aggravation. Neither the the pathogenic mechanism by which SARS-CoV-2 infects host cells, nor the host immune response to its infection have been fully understood, hence further studies are needed to give further evidence about these two phenomena. Keywords: COVID-19, SARS-CoV-2, Coronavirus, Structural proteins, Immune response.

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27

Sekenova, A., and V. Ogay. "Role of mesenchymal stem cells in the regulation of immune response." BULLETIN of the L.N. Gumilyov Eurasian National University. BIOSCIENCE Series 123, no. 2 (2018): 69–83. http://dx.doi.org/10.32523/2616-7034-2018-123-2-69-83.

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28

Thabit, Sandford. "Current Studies of Immunotherapy for glioblastoma triggers a measurable immune response." Psychology and Mental Health Care 2, no. 3 (July 1, 2018): 01–06. http://dx.doi.org/10.31579/2637-8892/029.

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29

Dimayuga, Paul C., Kuang-Yuh Chyu, and Bojan Cercek. "Immune responses regulating the response to vascular injury." Current Opinion in Lipidology 21, no. 5 (October 2010): 416–21. http://dx.doi.org/10.1097/mol.0b013e32833cacbe.

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30

Hartman, Zachary, Xiao Yi Yang, Gangjun Lei, Andrea Amalfitano, Michael Morse, Herbert Kim Lyerly, and Tim Clay. "Modulation of adenoviral vector immune responses through the over-expression of immune adaptor and viral immuno-modulatory genes (48.17)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S77—S78. http://dx.doi.org/10.4049/jimmunol.178.supp.48.17.

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Abstract For the past two decades, adenoviral vector platforms have been used as both gene therapy vehicles and vaccine platforms in various human clinical trials. However, the use of these, as well as other viral vector platforms, has been tempered by the innate immune and adaptive immune responses elicited. Despite the development of advanced generation adenoviral vectors, the innate responses precipitated by these vectors have remained largely unchanged due to the particular nature of the viral capsid and infectious process. To more effectively use these vectors for different purposes, we constructed adenoviral vectors encoding overexpression cassettes for various TLR adaptors (MyD88 and TRIF), RIG-I pathway adaptor (MAVS), as well as immuno-modulatory viral genes (pp65) whose expression might accentuate or inhibit the innate immune response enabled by adenoviral infection. Our studies show that while all of these immuno-modulatory vectors were able to effectively enhance (TLR and MAVS vectors) or inhibit (pp65 vectors) the NF-kB and IFN-beta responses in vitro, only certain vectors were able to affect the adaptive responses elicited in vivo. While our findings show that vector manipulation can influence vector-specific innate and adaptive immune responses, they also offer evidence for the highly regulatory nature of the innate response, as evidenced by the limited impact of certain adaptor overexpression.

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31

Haig, David M., Jackie Thomson, Colin McInnes, Catherine McCaughan, Wendy Imlach, Andrew Mercer, and Stephen Fleming. "Orf virus immuno-modulation and the host immune response." Veterinary Immunology and Immunopathology 87, no. 3-4 (September 2002): 395–99. http://dx.doi.org/10.1016/s0165-2427(02)00087-9.

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32

Walczak, Aleksandra M. "Response in Immune Repertoires." Biophysical Journal 120, no. 3 (February 2021): 194a—195a. http://dx.doi.org/10.1016/j.bpj.2020.11.1338.

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33

Dean, Dwane H., Raymond N. Hiramoto, and Vithal K. Ghanta. "Modulation of Immune Response." Journal of Periodontology 58, no. 7 (July 1987): 498–500. http://dx.doi.org/10.1902/jop.1987.58.7.498.

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34

Suarez, Giovanni. "Immune response toH pylori." World Journal of Gastroenterology 12, no. 35 (2006): 5593. http://dx.doi.org/10.3748/wjg.v12.i35.5593.

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35

&NA;. "HIV Vaccine ??? Immune Response." Drugs in R & D 3, no. 6 (2002): 411–20. http://dx.doi.org/10.2165/00126839-200203060-00011.

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36

Vignieri, Sacha. "Reconfiguring an immune response." Science 369, no. 6511 (September 24, 2020): 1579.1–1579. http://dx.doi.org/10.1126/science.369.6511.1579-a.

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37

Koga, Tetsuya. "Immune Response in Dermatophytosis." Nippon Ishinkin Gakkai Zasshi 44, no. 4 (2003): 273–75. http://dx.doi.org/10.3314/jjmm.44.273.

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38

del Mar Casal, Maria, and Manuel Casal. "Immune Response to Mycobacteria." Current Immunology Reviews 7, no. 1 (February 1, 2011): 13–18. http://dx.doi.org/10.2174/157339511794474280.

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39

Iwaguchi, Takao, and Tadayoshi Matsuda. "Hyperthermia and Immune Response." Thermal Medicine(Japanese Journal of Hyperthermic Oncology) 6, no. 1 (1990): 19–28. http://dx.doi.org/10.3191/thermalmedicine.6.19.

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40

Sander, Ruth. "Exercise boosts immune response." Nursing Older People 24, no. 6 (June 29, 2012): 11. http://dx.doi.org/10.7748/nop.24.6.11.s11.

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41

Novikova, I. A. "IRON AND IMMUNE RESPONSE." Health and Ecology Issues, no. 4 (December 28, 2011): 42–48. http://dx.doi.org/10.51523/2708-6011.2011-8-4-7.

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The present-day data on possible pathways of iron influence on human immune response and susceptibility to infections have been considered. The article describes changes of immunologic resistance in conditions of low iron level and mechanisms of iron status disturbance as a consequence of immunostimulation.

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42

Siu, Venus WS. "Sepsis and immune response." World Journal of Emergency Medicine 2, no. 2 (2011): 99. http://dx.doi.org/10.5847/wjem.j.issn.1920-8642.2011.02.004.

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43

Cai, Xiao-fang. "Sepsis and immune response." World Journal of Emergency Medicine 2, no. 2 (2011): 117. http://dx.doi.org/10.5847/wjem.j.issn.1920-8642.2011.02.007.

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44

Ren, Hong-sheng. "Sepsis and immune response." World Journal of Emergency Medicine 2, no. 2 (2011): 127. http://dx.doi.org/10.5847/wjem.j.issn.1920-8642.2011.02.009.

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45

&NA;. "Zidovudine lowers immune response?" Inpharma Weekly &NA;, no. 887 (May 1993): 7. http://dx.doi.org/10.2165/00128413-199308870-00013.

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46

Akilov, OE, and KY Mumcuoglu. "Immune response in demodicosis." Journal of the European Academy of Dermatology and Venereology 18, no. 4 (July 2004): 440–44. http://dx.doi.org/10.1111/j.1468-3083.2004.00964.x.

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47

Han, Jae Pil, and Su Jin Hong. "Immune Response toHelicobacter pyloriInfection." Korean Journal of Helicobacter and Upper Gastrointestinal Research 13, no. 4 (2013): 220. http://dx.doi.org/10.7704/kjhugr.2013.13.4.220.

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48

Sedwick, Caitlin. "Imaging the immune response." Journal of Cell Biology 179, no. 3 (October 22, 2007): 362. http://dx.doi.org/10.1083/jcb.1793rr1.

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49

&NA;, &NA;. "Pathogenesis and immune response." Current Opinion in Infectious Diseases 5, no. 3 (June 1992): 469–84. http://dx.doi.org/10.1097/00001432-199206000-00025.

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50

&NA;, &NA;. "Pathogenesis and immune response." Current Opinion in Infectious Diseases 8, no. 3 (June 1995): B87. http://dx.doi.org/10.1097/00001432-199506000-00016.

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