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Journal articles on the topic 'Host Immune Respose'

Author: Grafiati

Published: 6 September 2023

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1

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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2

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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3

Roilides, Emmanuel, Emmanuel Roilides, Maria Simitsopoulou, Aspasia Katragkou, and Thomas J. Walsh. "Host immune response againstScedosporiumspecies." Medical Mycology 47, no. 4 (January 2009): 433–40. http://dx.doi.org/10.1080/13693780902738006.

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4

Trasia, Reqgi First. "Host Immune Response to Malaria." International Islamic Medical Journal 2, no. 2 (July 28, 2021): 67–71. http://dx.doi.org/10.33086/iimj.v2i2.1681.

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Malaria is still a health threat, especially for children and pregnant women in endemic areas. The World Health Organization (WHO) reports 228 million cases of malaria occur worldwide and an estimated 405,000 deaths from malaria globally in 2018. A series of malaria control efforts according to WHO recommendations have been carried out widely. However, these programs face obstacles. Therefore, the existence of an effective malaria vaccine is absolutely necessary in a series of malaria control strategies. Development of a malaria vaccine requires a basic concept regarding the host's immune response to malaria. Unfortunately, only a few in Indonesia have reviewed how the immune response is. This article will present an understanding of how the human immune system responds to Plasmodium falciparum.

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Cheng, E. "Imaging the Host Immune Response." Science Translational Medicine 2, no. 40 (July 13, 2010): 40ec113. http://dx.doi.org/10.1126/scitranslmed.3001469.

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6

Li, Chaozheng, Shaoping Weng, and Jianguo He. "WSSV–host interaction: Host response and immune evasion." Fish & Shellfish Immunology 84 (January 2019): 558–71. http://dx.doi.org/10.1016/j.fsi.2018.10.043.

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7

Bhopale, Mahendra. "Experimental Hookworm Infection in Laboratory animals: Parasite behavior, Immune response and Chemotherapeutic Studies." Biotechnology and Bioprocessing 2, no. 5 (June 24, 2021): 01–03. http://dx.doi.org/10.31579/2766-2314/040.

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Hookworm disease is known to be caused allergic manifestation and severe anemic pathogenicity in man and canine hosts. Attempts have been made to establish laboratory models of Necator americaus, Ancylostoma duodenale, and Ancylostoma ceylanicum, together with canine parasite, Ancylostoma caninum. The studies include pathophysiological aspects of the host-parasite relationship, and develop to establish patent infection. Immunological approach to selecting antigen for diagnosis and protective immunity purpose using larval and adult worm antigens and their secretions became the focus with the subsequent discovery of cloning in vaccine development as main research interest. Chemotherapy of newer drug screening in laboratory models ultimately selected to use for preventive chemotherapy in hookworm endemic areas using recommended drugs.

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8

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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9

Elaskandrany, Miar, Rohin Patel, Mintoo Patel, George Miller, Deepak Saxena, and Anjana Saxena. "Fungi, host immune response, and tumorigenesis." American Journal of Physiology-Gastrointestinal and Liver Physiology 321, no. 2 (August 1, 2021): G213—G222. http://dx.doi.org/10.1152/ajpgi.00025.2021.

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Advances in -omics analyses have tremendously enhanced our understanding of the role of the microbiome in human health and disease. Most research is focused on the bacteriome, but scientists have now realized the significance of the virome and microbial dysbiosis as well, particularly in noninfectious diseases such as cancer. In this review, we summarize the role of mycobiome in tumorigenesis, with a dismal prognosis, and attention to pancreatic ductal adenocarcinoma (PDAC). We also discuss bacterial and mycobial interactions to the host’s immune response that is prevalently responsible for resistance to cancer therapy, including immunotherapy. We reported that the Malassezia species associated with scalp and skin infections, colonize in human PDAC tumors and accelerate tumorigenesis via activating the C3 complement-mannose-binding lectin (MBL) pathway. PDAC tumors thrive in an immunosuppressive microenvironment with desmoplastic stroma and a dysbiotic microbiome. Host-microbiome interactions in the tumor milieu pose a significant threat in driving the indolent immune behavior of the tumor. Microbial intervention in multimodal cancer therapy is a promising novel approach to modify an immunotolerant (“cold”) tumor microenvironment to an immunocompetent (“hot”) milieu that is effective in eliminating tumorigenesis.

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10

Visser, Douwe H., Regan S. Solomons, Katharina Ronacher, Gijs T. van Well, Martijn W. Heymans, Gerhard Walzl, Novel N. Chegou, Johan F. Schoeman, and Anne M. van Furth. "Host Immune Response to Tuberculous Meningitis." Clinical Infectious Diseases 60, no. 2 (October 9, 2014): 177–87. http://dx.doi.org/10.1093/cid/ciu781.

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11

Solomon, Katie. "The host immune response toClostridium difficileinfection." Therapeutic Advances in Infectious Disease 1, no. 1 (February 2013): 19–35. http://dx.doi.org/10.1177/2049936112472173.

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12

Boyartchuk, V., and W. Dietrich. "Genetic dissection of host immune response." Genes & Immunity 3, no. 3 (May 2002): 119–22. http://dx.doi.org/10.1038/sj.gene.6363843.

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13

SCHLUGER, NEIL W, and WILLIAM N ROM. "The Host Immune Response to Tuberculosis." American Journal of Respiratory and Critical Care Medicine 157, no. 3 (March 1998): 679–91. http://dx.doi.org/10.1164/ajrccm.157.3.9708002.

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14

Moonah, Shannon N., Nona M. Jiang, and William A. Petri. "Host Immune Response to Intestinal Amebiasis." PLoS Pathogens 9, no. 8 (August 22, 2013): e1003489. http://dx.doi.org/10.1371/journal.ppat.1003489.

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15

Inman, R. D. "Immunogenetic aspects of host immune response." Canadian Journal of Microbiology 34, no. 3 (March 1, 1988): 319–22. http://dx.doi.org/10.1139/m88-058.

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The central role of histocompatibility leukocyte antigens (HLA) class II molecules in antigen presentation has received great attention in recent years, yet class I molecules have been defined as primarily functioning as a restriction element for cytotoxic T cell killing of virus-infected cells. Extensive clinical evidence, however, indicates that the HLA class I genes are strongly associated with nonseptic complications of enteric and genitourinary bacterial infections. Ninety percent of patients with Reiter's syndrome and reactive arthritis are positive for HLA-B27, yet the mechanism of disease susceptibility conferred by this gene remains obscure. Hypotheses concerning this interaction include (i) class I antigens functioning as receptors for microbial antigens; (ii) class I antigens expressing determinants that cross-react with microbial antigens; and (iii) class I genes controlling immunoregulatory functions that dictate qualitative differences in immune response to pathogenic organisms. These hypotheses await formal testing and hold great promise for understanding immunogenetic control of immune responses in general.

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16

Sana, Madiha, Muhammad Rashid, Imran Rashid, Haroon Akbar, Jorge E. Gomez-Marin, and Isabelle Dimier-Poisson. "Immune response against toxoplasmosis—some recent updates RH: Toxoplasma gondii immune response." International Journal of Immunopathology and Pharmacology 36 (January 2022): 039463202210784. http://dx.doi.org/10.1177/03946320221078436.

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Aims Cytokines, soluble mediators of immunity, are key factors of the innate and adaptive immune system. They are secreted from and interact with various types of immune cells to manipulate host body’s immune cell physiology for a counter-attack on the foreign body. A study was designed to explore the mechanism of Toxoplasma gondii ( T. gondii) resistance from host immune response. Methods and results The published data on aspect of host (murine and human) immune response against T. gondii was taken from Google scholar and PubMed. Most relevant literature was included in this study. The basic mechanism of immune response starts from the interactions of antigens with host immune cells to trigger the production of cytokines (pro-inflammatory and anti-inflammatory) which then act by forming a cytokinome (network of cytokine). Their secretory equilibrium is essential for endowing resistance to the host against infectious diseases, particularly toxoplasmosis. A narrow balance lying between Th1, Th2, and Th17 cytokines (as demonstrated until now) is essential for the development of resistance against T. gondii as well as for the survival of host. Excessive production of pro-inflammatory cytokines leads to tissue damage resulting in the production of anti-inflammatory cytokines which enhances the proliferation of Toxoplasma. Stress and other infectious diseases (human immunodeficiency virus (HIV)) that weaken the host immunity particularly the cellular component, make the host susceptible to toxoplasmosis especially in pregnant women. Conclusion The current review findings state that in vitro harvesting of IL12 from DCs, Np and MΦ upon exposure with T. gondii might be a source for therapeutic use in toxoplasmosis. Current review also suggests that therapeutic interventions leading to up-regulation/supplementation of SOCS-3, IL12, and IFNγ to the infected host could be a solution to sterile immunity against T. gondii infection. This would be of interest particularly in patients passing through immunosuppression owing to any reason like the ones receiving anti-cancer therapy, the ones undergoing immunosuppressive therapy for graft/transplantation, the ones suffering from immunodeficiency virus (HIV) or having AIDS. Another imortant suggestion is to launch the efforts for a vaccine based on GRA6Nt or other similar antigens of T. gondii as a probable tool to destroy tissue cysts.

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17

Korobeinikov, Andrei. "Immune response and within-host viral evolution: Immune response can accelerate evolution." Journal of Theoretical Biology 456 (November 2018): 74–83. http://dx.doi.org/10.1016/j.jtbi.2018.08.003.

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18

Surbatovic, Maja, Milic Veljovic, Jasna Jevdjic, Nada Popovic, Dragan Djordjevic, and Sonja Radakovic. "Immunoinflammatory Response in Critically Ill Patients: Severe Sepsis and/or Trauma." Mediators of Inflammation 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/362793.

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Immunoinflammatory response in critically ill patients is very complex. This review explores some of the new elements of immunoinflammatory response in severe sepsis, tumor necrosis factor-alpha in severe acute pancreatitis as a clinical example of immune response in sepsis, immune response in severe trauma with or without secondary sepsis, and genetic aspects of host immuno-inflammatory response to various insults in critically ill patients.

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19

Brunham, R. C., F. A. Plummer, and R. S. Stephens. "Bacterial antigenic variation, host immune response, and pathogen-host coevolution." Infection and Immunity 61, no. 6 (1993): 2273–76. http://dx.doi.org/10.1128/iai.61.6.2273-2276.1993.

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20

Musundi, Beryl. "An immuno-epidemiological model linking between-host and within-host dynamics of cholera." Mathematical Biosciences and Engineering 20, no. 9 (2023): 16012–30. http://dx.doi.org/10.3934/mbe.2023714.

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<abstract><p>Cholera, a severe gastrointestinal infection caused by the bacterium <italic>Vibrio cholerae</italic>, remains a major threat to public health, with a yearly estimated global burden of 2.9 million cases. Although most existing models for the disease focus on its population dynamics, the disease evolves from within-host processes to the population, making it imperative to link the multiple scales of the disease to gain better perspectives on its spread and control. In this study, we propose an immuno-epidemiological model that links the between-host and within-host dynamics of cholera. The immunological (within-host) model depicts the interaction of the cholera pathogen with the adaptive immune response. We distinguish pathogen dynamics from immune response dynamics by assigning different time scales. Through a time-scale analysis, we characterise a single infected person by their immune response. Contrary to other within-host models, this modelling approach allows for recovery through pathogen clearance after a finite time. Then, we scale up the dynamics of the infected person to construct an epidemic model, where the infected population is structured by individual immunological dynamics. We derive the basic reproduction number ($ \mathcal{R}_0 $) and analyse the stability of the equilibrium points. At the disease-free equilibrium, the disease will either be eradicated if $ \mathcal{R}_0 < 1 $ or otherwise persists. A unique endemic equilibrium exists when $ \mathcal{R}_0 > 1 $ and is locally asymptotically stable without a loss of immunity.</p></abstract>

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21

Buldain, Idoia, Leire Martin-Souto, Aitziber Antoran, Maialen Areitio, Leire Aparicio-Fernandez, Aitor Rementeria, Fernando L. Hernando, and Andoni Ramirez-Garcia. "The Host Immune Response to Scedosporium/Lomentospora." Journal of Fungi 7, no. 2 (January 22, 2021): 75. http://dx.doi.org/10.3390/jof7020075.

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Infections caused by the opportunistic pathogens Scedosporium/Lomentospora are on the rise. This causes problems in the clinic due to the difficulty in diagnosing and treating them. This review collates information published on immune response against these fungi, since an understanding of the mechanisms involved is of great interest in developing more effective strategies against them. Scedosporium/Lomentospora cell wall components, including peptidorhamnomannans (PRMs), α-glucans and glucosylceramides, are important immune response activators following their recognition by TLR2, TLR4 and Dectin-1 and through receptors that are yet unknown. After recognition, cytokine synthesis and antifungal activity of different phagocytes and epithelial cells is species-specific, highlighting the poor response by microglial cells against L. prolificans. Moreover, a great number of Scedosporium/Lomentospora antigens have been identified, most notably catalase, PRM and Hsp70 for their potential medical applicability. Against host immune response, these fungi contain evasion mechanisms, inducing host non-protective response, masking fungal molecular patterns, destructing host defense proteins and decreasing oxidative killing. In conclusion, although many advances have been made, many aspects remain to be elucidated and more research is necessary to shed light on the immune response to Scedosporium/Lomentospora.

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Helisa, Yasmin Nur, and Horizon Winangkoso. "Adopting Natural Host Immune Response Against Zoonosis." Journal of Education, Management and Development Studies 2, no. 1 (March 15, 2022): 52–66. http://dx.doi.org/10.52631/jemds.v2i1.67.

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Zoonosis originated from the transmission of pathogens between species. Rapid mutation causes the pathogens to develop resistance to treatments. Thus, there is an urgent need for medications that could maintain efficacy when encountering new strains. This study aims to discern the possibility of overcoming threats from EIDs by recreating immune responses of natural hosts and reinforcing them in the human system. The methodology used is literature study, as the resarcher utilized data presented by similar studies. References will be taken from clinical trials and studies on related topics from PubMed, ResearchGate, and NCBI. Within multiple research papers, it was found that several experts support the idea of mimicking hosts' immunity through the use of interferon. Treatments with IFN-2b significantly reduce viral infection of SARS-CoV-2 in the upper respiratory tract and increase blood levels of inflammatory markers, according to research conducted in Wuhan. Similar results apply in other trials, proving that interferon managed to contain the invasion of pathogens. This is shown through a reduction in the severity of infections, the duration of viral clearance, and levels of mortality. The results conclude that the use of interferon benefits the patient’s recovery progress by mimicking the natural host’s immune response and heightening the viral clearance rate. More research needs to be done to explore the effect of excessive IFN-$\alpha$/$\beta$ usage on immunity.

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23

Lambert, Paul H., Giuseppe del Giudice, and Georges E. Grau. "Host immune response and immunopathology in malaria." Memórias do Instituto Oswaldo Cruz 81, suppl 2 (1986): 185–90. http://dx.doi.org/10.1590/s0074-02761986000600030.

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Sabia, C., M. L. Montesano, and C. Napoli. "Transplantation and host immune response toToxoplasma gondii." Transplant Infectious Disease 15, no. 3 (March 28, 2013): E124—E125. http://dx.doi.org/10.1111/tid.12076.

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25

Dubin, Patricia J., and Jay K. Kolls. "Pseudomonas aeruginosaand the host pulmonary immune response." Expert Review of Respiratory Medicine 1, no. 1 (August 2007): 121–37. http://dx.doi.org/10.1586/17476348.1.1.121.

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26

Stapleton, J. T. "Host Immune Response To Hepatitis A Virus." Journal of Infectious Diseases 171, Supplement 1 (March 1, 1995): S9—S14. http://dx.doi.org/10.1093/infdis/171.supplement_1.s9.

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27

Navarro, C. "Predation risk, host immune response, and parasitism." Behavioral Ecology 15, no. 4 (July 1, 2004): 629–35. http://dx.doi.org/10.1093/beheco/arh054.

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28

Christiaansen, Allison, Steven M. Varga, and Juliet V. Spencer. "Viral manipulation of the host immune response." Current Opinion in Immunology 36 (October 2015): 54–60. http://dx.doi.org/10.1016/j.coi.2015.06.012.

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Bhatt, Kamlesh, and Padmini Salgame. "Host Innate Immune Response to Mycobacterium tuberculosis." Journal of Clinical Immunology 27, no. 4 (March 16, 2007): 347–62. http://dx.doi.org/10.1007/s10875-007-9084-0.

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Petry, Franz, Vera Jakobi, and Tesfaye S. Tessema. "Host immune response to Cryptosporidium parvum infection." Experimental Parasitology 126, no. 3 (November 2010): 304–9. http://dx.doi.org/10.1016/j.exppara.2010.05.022.

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Apt, A., and T. K. Kondratieva. "Tuberculosis: Pathogenesis, immune response, and host genetics." Molecular Biology 42, no. 5 (October 2008): 784–93. http://dx.doi.org/10.1134/s0026893308050154.

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Kelly, Ciarán P., and Lorraine Kyne. "The host immune response to Clostridium difficile." Journal of Medical Microbiology 60, no. 8 (August 1, 2011): 1070–79. http://dx.doi.org/10.1099/jmm.0.030015-0.

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Rello, Jordi, and RichardR Watkins. "Monitoring the Host Immune Response in Sepsis." Journal of Translational Critical Care Medicine 4, no. 1 (2022): 18. http://dx.doi.org/10.4103/jtccm-d-22-00013.

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Sharma, Tarina, Anwar Alam, Aquib Ehtram, Anshu Rani, Sonam Grover, Nasreen Z. Ehtesham, and Seyed E. Hasnain. "The Mycobacterium tuberculosis PE_PGRS Protein Family Acts as an Immunological Decoy to Subvert Host Immune Response." International Journal of Molecular Sciences 23, no. 1 (January 4, 2022): 525. http://dx.doi.org/10.3390/ijms23010525.

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Mycobacterium tuberculosis (M.tb) is a successful pathogen that can reside within the alveolar macrophages of the host and can survive in a latent stage. The pathogen has evolved and developed multiple strategies to resist the host immune responses. M.tb escapes from host macrophage through evasion or subversion of immune effector functions. M.tb genome codes for PE/PPE/PE_PGRS proteins, which are intrinsically disordered, redundant and antigenic in nature. These proteins perform multiple functions that intensify the virulence competence of M.tb majorly by modulating immune responses, thereby affecting immune mediated clearance of the pathogen. The highly repetitive, redundant and antigenic nature of PE/PPE/PE_PGRS proteins provide a critical edge over other M.tb proteins in terms of imparting a higher level of virulence and also as a decoy molecule that masks the effect of effector molecules, thereby modulating immuno-surveillance. An understanding of how these proteins subvert the host immunological machinery may add to the current knowledge about M.tb virulence and pathogenesis. This can help in redirecting our strategies for tackling M.tb infections.

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Fremder, Ella, Eyal Jacob, Irena Khononov, Eran Issler, Shani Raveh, Nili Dahan, Haim Bar, and Yuval Shaked. "The host response to immune checkpoint inhibitors: From mechanisms to therapeutic implications." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e14584-e14584. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e14584.

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e14584 Background: One of the major challenges in clinical immuno-oncology today is predicting which patients will respond to treatment. Although the use of immune checkpoint inhibitors (ICIs) has significantly improved therapeutic outcomes in a subset of patients with advanced malignancies, the majority of patients do not respond to treatment and some even hyper-progress. This response pattern raises questions regarding the possible mechanisms of resistance to ICIs. In the last decade we and others have shown that the host, in response to almost any type of anti-cancer drug, generates pro-tumorigenic and pro-metastatic effects which in turn contribute to tumor relapse and resistance to therapy despite an initial response. However, such host effects have never been investigated using immune-oncology drugs. Methods: We used functional and computational methods on plasma samples from both mouse models and cancer patients to identify the host-mediated tumor promoting molecular pathways that are induced in response to ICI therapy. Results: We found that these pathways are composed of dominant factors that regulate pro-inflammatory, metastatic and proliferation activities and thus contribute to rapid tumor re-growth. In pre-clinical models, we have found that pharmacological blockade of specific dominant factors overcomes the tumor-promoting effects induced by the host in response to ICI therapy. Conclusions: Based on our collective findings, we propose that therapies inhibiting host-mediated pro-tumorigenic effects could be used in combination with ICIs as a strategy to minimize tumor hyper-progression and increase the susceptibility of resistant tumors to ICI therapy. Furthermore, our studies pave the way towards the discovery of new predictive biomarkers for identifying subjects who will benefit from ICI therapy.

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Notari, Luigi, Aiping Zhao, Jennifer A. Stiltz, Shu Yan, Jaladanki N. Rao, Joseph F. Urban, and Terez Shea-Donohue. "T1770 Enteric Nematodes Regulates Host Proteolytic Pathway on Immune Cells: Influence on Host Immune Response." Gastroenterology 138, no. 5 (May 2010): S—575. http://dx.doi.org/10.1016/s0016-5085(10)62648-0.

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37

Näpflin, Kathrin, and Paul Schmid-Hempel. "Immune response and gut microbial community structure in bumblebees after microbiota transplants." Proceedings of the Royal Society B: Biological Sciences 283, no. 1831 (May 25, 2016): 20160312. http://dx.doi.org/10.1098/rspb.2016.0312.

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Microbial communities are a key component of host health. As the microbiota is initially ‘foreign’ to a host, the host's immune system should respond to its acquisition. Such variation in the response should relate not only to host genetic background, but also to differences in the beneficial properties of the microbiota. However, little is known about such interactions. Here, we investigate the gut microbiota of the bumblebee, Bombus terrestris , which has a protective function against the bee's natural trypanosome gut parasite, Crithidia bombi . We transplanted ‘resistant’ and ‘susceptible’ microbiota into ‘resistant’ and ‘susceptible’ host backgrounds, and studied the activity of the host immune system. We found that bees from different resistance backgrounds receiving a microbiota differed in aspects of their immune response. At the same time, the elicited immune response also depended on the received microbiota's resistance phenotype. Furthermore, the microbial community composition differed between microbiota resistance phenotypes (resistant versus susceptible). Our results underline the complex feedback between the host's ability to potentially exert selection on the establishment of a microbial community and the influence of the microbial community on the host immune response in turn.

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Riley, Patrick. "Overcoming the problem of the lack of an immune response to cancer: A possible haptogenic approach to cancer immunotherapy." Cancer Research and Cellular Therapeutics 5, no. 1 (February 12, 2021): 01–04. http://dx.doi.org/10.31579/2640-1053/072.

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Cancer cells possess a number of unusual features, most of which are explicable in the light of the theory of epigenetic carcinogenesis. This includes the remarkable failure of malignant cells to evoke an immunological response from the host which is ascribed to their deviant behaviour resulting from anomalous expression of normal gene products. Given this background a possible approach to eliciting a specific anti-cancer immune response is proposed which involves selective haptenation of an identifiable target protein.

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Horak, Richard D., Sean P. Leonard, and Nancy A. Moran. "Symbionts shape host innate immunity in honeybees." Proceedings of the Royal Society B: Biological Sciences 287, no. 1933 (August 26, 2020): 20201184. http://dx.doi.org/10.1098/rspb.2020.1184.

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The gut microbiome plays a critical role in the health of many animals. Honeybees are no exception, as they host a core microbiome that affects their nutrition and immune function. However, the relationship between the honeybee immune system and its gut symbionts is poorly understood. Here, we explore how the beneficial symbiont Snodgrassella alvi affects honeybee immune gene expression. We show that both live and heat-killed S. alvi protect honeybees from the opportunistic pathogen Serratia marcescens and lead to the expression of host antimicrobial peptides . Honeybee immune genes respond differently to live S. alvi compared to heat-killed S. alvi, the latter causing a more extensive immune expression response. We show a preference for Toll pathway upregulation over the Imd pathway in the presence of both live and heat-killed S. alvi . Finally, we find that live S. alvi aids in clearance of S. marcescens from the honeybee gut, supporting a potential role for the symbiont in colonization resistance. Our results show that colonization by the beneficial symbiont S. alvi triggers a replicable honeybee immune response. These responses may benefit the host and the symbiont, by helping to regulate gut microbial members and preventing overgrowth or invasion by opportunists.

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Abès, Riad, Sébastien Héritier, Charles-Antoine Dutertre, and Jean-Luc Teillaud. "Immune control of tumors: host immune response and antibody-based immunotherapy." Biomedicine & Pharmacotherapy 62, no. 8 (October 2008): 516. http://dx.doi.org/10.1016/j.biopha.2008.07.066.

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Moller, Anders Pape, and Johannes Erritzoe. "Parasite Virulence and Host Immune Defense: Host Immune Response is Related to Nest Reuse in Birds." Evolution 50, no. 5 (October 1996): 2066. http://dx.doi.org/10.2307/2410763.

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Møller, Anders Pape, and Johannes Erritzøe. "PARASITE VIRULENCE AND HOST IMMUNE DEFENSE: HOST IMMUNE RESPONSE IS RELATED TO NEST REUSE IN BIRDS." Evolution 50, no. 5 (October 1996): 2066–72. http://dx.doi.org/10.1111/j.1558-5646.1996.tb03592.x.

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Steain, Megan, Barry Slobedman, and Allison Abendroth. "The host immune response to varicella zoster virus." Future Virology 7, no. 12 (December 2012): 1205–20. http://dx.doi.org/10.2217/fvl.12.116.

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Hayashi, K. "Host immune response to herpes simplex virus infections." Uirusu 39, no. 1 (1989): 1–19. http://dx.doi.org/10.2222/jsv.39.1.

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Raveendran, Ranjith. "“Adapting to terminologies involved in host immune response”." IOSR Journal of Dental and Medical Sciences 11, no. 2 (2013): 01–05. http://dx.doi.org/10.9790/0853-1120105.

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Sausen, Daniel, Kirstin Reed, Maimoona Bhutta, Elisa Gallo, and Ronen Borenstein. "Evasion of the Host Immune Response by Betaherpesviruses." International Journal of Molecular Sciences 22, no. 14 (July 13, 2021): 7503. http://dx.doi.org/10.3390/ijms22147503.

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The human immune system boasts a diverse array of strategies for recognizing and eradicating invading pathogens. Human betaherpesviruses, a highly prevalent subfamily of viruses, include human cytomegalovirus (HCMV), human herpesvirus (HHV) 6A, HHV-6B, and HHV-7. These viruses have evolved numerous mechanisms for evading the host response. In this review, we will highlight the complex interplay between betaherpesviruses and the human immune response, focusing on protein function. We will explore methods by which the immune system first responds to betaherpesvirus infection as well as mechanisms by which viruses subvert normal cellular functions to evade the immune system and facilitate viral latency, persistence, and reactivation. Lastly, we will briefly discuss recent advances in vaccine technology targeting betaherpesviruses. This review aims to further elucidate the dynamic interactions between betaherpesviruses and the human immune system.

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Khadela, Avinash, Vivek P. Chavda, Humzah Postwala, Yesha Shah, Priya Mistry, and Vasso Apostolopoulos. "Epigenetics in Tuberculosis: Immunomodulation of Host Immune Response." Vaccines 10, no. 10 (October 18, 2022): 1740. http://dx.doi.org/10.3390/vaccines10101740.

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Tuberculosis is a stern, difficult to treat chronic infection caused by acid-fast bacilli that tend to take a long time to be eradicated from the host’s environment. It requires the action of both innate and adaptive immune systems by the host. There are various pattern recognition receptors present on immune cells, which recognize foreign pathogens or its product and trigger the immune response. The epigenetic modification plays a crucial role in triggering the susceptibility of the host towards the pathogen and activating the host’s immune system against the invading pathogen. It alters the gene expression modifying the genetic material of the host’s cell. Epigenetic modification such as histone acetylation, alteration in non-coding RNA, DNA methylation and alteration in miRNA has been studied for their influence on the pathophysiology of tuberculosis to control the spread of infection. Despite several studies being conducted, many gaps still exist. Herein, we discuss the immunopathophysiological mechanism of tuberculosis, the essentials of epigenetics and the recent encroachment of epigenetics in the field of tuberculosis and its influence on the outcome and pathophysiology of the infection.

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Wang, Rui, Yuta Hozumi, Yong-Hui Zheng, Changchuan Yin, and Guo-Wei Wei. "Host Immune Response Driving SARS-CoV-2 Evolution." Viruses 12, no. 10 (September 27, 2020): 1095. http://dx.doi.org/10.3390/v12101095.

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The transmission and evolution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are of paramount importance in controlling and combating the coronavirus disease 2019 (COVID-19) pandemic. Currently, over 15,000 SARS-CoV-2 single mutations have been recorded, which have a great impact on the development of diagnostics, vaccines, antibody therapies, and drugs. However, little is known about SARS-CoV-2’s evolutionary characteristics and general trend. In this work, we present a comprehensive genotyping analysis of existing SARS-CoV-2 mutations. We reveal that host immune response via APOBEC and ADAR gene editing gives rise to near 65% of recorded mutations. Additionally, we show that children under age five and the elderly may be at high risk from COVID-19 because of their overreaction to the viral infection. Moreover, we uncover that populations of Oceania and Africa react significantly more intensively to SARS-CoV-2 infection than those of Europe and Asia, which may explain why African Americans were shown to be at increased risk of dying from COVID-19, in addition to their high risk of COVID-19 infection caused by systemic health and social inequities. Finally, our study indicates that for two viral genome sequences of the same origin, their evolution order may be determined from the ratio of mutation type, C > T over T > C.

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Uno, Naoko, and Ted M. Ross. "Dengue virus and the host innate immune response." Emerging Microbes & Infections 7, no. 1 (October 10, 2018): 1–11. http://dx.doi.org/10.1038/s41426-018-0168-0.

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Baillie, J. K. "Targeting the host immune response to fight infection." Science 344, no. 6186 (May 22, 2014): 807–8. http://dx.doi.org/10.1126/science.1255074.

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