• IMMUNE NETWORK
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• v.23 no.2
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• pp.19.1-19.10
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• 2023

Endemic human coronaviruses (HCoVs) have been evidenced to be cross-reactive to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although a correlation exists between the immunological memory to HCoVs and coronavirus disease 2019 (COVID-19) severity, there is little experimental evidence for the effects of HCoV memory on the efficacy of COVID-19 vaccines. Here, we investigated the Ag-specific immune response to COVID-19 vaccines in the presence or absence of immunological memory against HCoV spike Ags in a mouse model. Pre-existing immunity against HCoV did not affect the COVID-19 vaccine-mediated humoral response with regard to Ag-specific total IgG and neutralizing Ab levels. The specific T cell response to the COVID-19 vaccine Ag was also unaltered, regardless of pre-exposure to HCoV spike Ags. Taken together, our data suggest that COVID-19 vaccines elicit comparable immunity regardless of immunological memory to spike of endemic HCoVs in a mouse model.

• IMMUNE NETWORK
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• v.3 no.2
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• pp.110-117
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• 2003

Background: The usefulness of DNA vaccine at priming step of heterologous prime-boost vaccination led to DNA vaccine closer to practical reality. DNA vaccine priming followed by recombinant viral vector boosting via systemic route induces optimal systemic immunity but no mucosal immunity. Mucosal vaccination of the reversed protocol (recombinant viral vector priming-DNA vaccine boosting), however, can induce both maximal mucosal and systemic immunity. Here, we tried to address the reason why the mucosal protocol of prime-boost vaccination differs from that of systemic vaccination. Methods: To address the importance of primary immunity induced at priming step, mice were primed with different doses of DNA vaccine or coadministration of DNA vaccine plus mucosal adjuvant, and immunity including serum IgG and mucosal IgA was then determined following boosting with recombinant viral vector. Next, to assess influence of humoral pre-existing immunity on boosting $CD8^+$ T cell-mediated immunity, $CD8^+$ T cell-mediated immunity in B cell-deficient (${\mu}K/O$) mice immunized with prime-boost regimens was evaluated by CTL assay and $IFN-{\gamma}$-producing cells. Results: Immunity primed with recombinant viral vector was effectively boosted with DNA vaccine even 60 days later. In particular, animals primed by increasing doses of DNA vaccine or incorporating an adjuvant at priming step and boosted by recombinant viral vector elicited comparable responses to recombinant viral vector primed-DNA vaccine boosted group. Humoral pre-existing immunity was also unlikely to interfere the boosting effect of $CD8^+$ T cell-mediated immunity by recombinant viral vector. Conclusion: This report provides the important point that optimally primed responses should be considered in mucosal immunization of heterologous prime-boost regimens for inducing the effective boosting at both mucosal and systemic sites.

• IMMUNE NETWORK
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• v.24 no.4
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• pp.28.1-28.13
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• 2024

Vaccines are the most effective intervention currently available, offering protective immunity against targeted pathogens. The emergence of the coronavirus disease 2019 pandemic has prompted rapid development and deployment of lipid nanoparticle encapsulated, mRNA-based vaccines. While these vaccines have demonstrated remarkable immunogenicity, concerns persist regarding their ability to confer durable protective immunity to continuously evolving severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants. This review focuses on human B cell responses induced by SARS-CoV-2 mRNA vaccination, with particular emphasis on the crucial role of germinal center reactions in shaping enduring protective immunity. Additionally, we explored observations of immunological imprinting and dynamics of recalled pre-existing immunity following variants of concern-based booster vaccination. Insights from this review contribute to comprehensive understanding B cell responses to mRNA vaccination in humans, thereby refining vaccination strategies for optimal and sustained protection against evolving coronavirus variants.

• IMMUNE NETWORK
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• v.14 no.6
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• pp.265-276
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• 2014

The interactions between B7 molecules and CD28-family receptors are crucial in the regulation of adaptive cellular immunity. In cancer, the aberrant expression of co-inhibitory B7 molecules has been attributed to reduced anti-tumor immunity and cancer immune evasion, prompting the development of cancer therapeutics that can restore T cell function. Murine tumor models have provided significant support for the targeting of multiple immune checkpoints involving CTLA-4, PD-1, ICOS, B7-H3 and B7-H4 during tumor growth, and clinical studies investigating the therapeutic effects of CTLA-4 and PD-1 blockade have shown exceptionally promising results in patients with advanced melanoma and other cancers. The expression pattern of co-inhibitory B7 ligands in the tumor microenvironment has also been largely correlated with poor patient prognosis, and recent evidence suggests that the presence of several B7 molecules may predict the responsiveness of immunotherapies that rely on pre-existing tumor-associated immune responses. While monotherapies blocking T cell co-inhibition have beneficial effects in reducing tumor burden, combinatorial immunotherapy targeting multiple immune checkpoints involved in various stages of the anti-tumor response has led to the most substantial impact on tumor reduction. In this review, we will examine the contributions of B7- and CD28-family members in the context of cancer development, and discuss the implications of current human findings in cancer immunotherapy.

• Korean Journal of Veterinary Service
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• v.44 no.4
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• pp.291-297
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• 2021

Severe outbreaks of porcine epidemic diarrhoea virus (PEDV) have continued to re-emerge worldwide. Because of the high mortality rate of suckling piglets in PEDV outbreaks, the disease causes significant economic losses in the pig industry. The limited pre-existing immunity against this virus is thought to cause an explosive increase in infection in pig farms. This study aimed to evaluate the clinical symptoms of PEDV after intentional exposure (feedback). During the first few days of the outbreak in a breeding pig farm, 14 sows showed watery diarrhoea, and the disease subsequently spread rapidly throughout the barn. Pigs that were intentionally exposed to PEDV (n=251) showed watery diarrhoea (46.6%), reduced appetite (17.5%), and vomiting (6.0%). However, 75 exposed pigs (29.9%) showed no clinical signs of disease. Four weeks after the feedback challenge, 34 sows gave birth to litters of piglets, which survived with no diarrhoea. Five weeks after the start of the outbreak, PEDV was not detected in any of the examined samples, including environmental swabs. Thus, early diagnosis, prompt establishment of herd immunity, and strict application of biosecurity are good practices to reduce the mortality rates among new-born piglets and control economic losses in pig farms showing PEDV outbreaks.

• Journal of Microbiology and Biotechnology
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• v.19 no.3
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• pp.307-313
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• 2009

In order to systemically investigate the possibility of using coxsackievirus B3 (CVB3) to deliver foreign genes in vivo, a recombinant strain of CVB3 encoding the renilla gene (CVB3-renilla) was constructed. The recombinant CVB3 resulted in extensive and transient expression of the renilla protein within mouse organs, especially the pancreas. The level of expression was generally dependent upon the viral titer present. Moreover, the CVB3-renilla strain was completely attenuated. Interestingly, the recombinant CVB3 vector was expressed much more strongly in mouse organs than was a comparable adenoviral vector. The CVB3-renilla strain did not express the renilla gene in mice with pre-existing coxsackievirus-specific neutralizing antibodies, but direct organ-specific administration of the virus during open-peritoneum surgery was able to circumvent this immunity. This coxsackievirus vector may represent a useful means for delivering and expressing foreign genes in mouse models in an acute and extensive fashion.

• Journal of Arbitration Studies
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• v.30 no.4
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• pp.121-138
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• 2020

The O2O services in the healthcare sector have only been in full swing for about three years, and unlike existing O2O consumer goods, the scale and scope of the dispute are more complicated due to restrictions on medical treatment. In this study, O2O service platform operators and medical institutions' roles and responsibilities were redefined as a countermeasure for resolving disputes in healthcare O2O services and the laws for changing the transaction environment. A change in institutional mechanisms was proposed. This study looked at the types of consumer disputes related to healthcare O2O services as insufficient information problems, problems in the course of medical service implementation, problems with immunity provisions for platform operators, cancellations, and non-compliance with refunds. All the information generated during transactions in the healthcare sector was extensive in scale and included the most sensitive information among personal information, stressing the importance of ensuring security. The area that started in the O2O range before the medical institution visit also proposed a plan to establish a system for the delivery of proven information as a pre-medical person. The scale and growth will grow faster, given that consumers can experience the information they want anytime, anywhere they want. However, the platform broker's role, a link player, will become more important because consumers who use the service will have their first meeting with non-face-to-face product providers. On the other hand, service providers may have side effects of misleading consumers by providing false information or misleading consumers through exaggerated advertisements. The O2O service market is expected to expand beyond distribution and dining out to the entire industry. However, since it is challenging to check accurate statistics on the detailed market, various disputes and consumer protection measures will be required for each detailed market, and comprehensive leading solutions will be essential in the future.

• Biomolecules & Therapeutics
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• v.30 no.1
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• pp.48-54
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• 2022

GPR43 (also known as FFAR2), a metabolite-sensing G-protein-coupled receptor stimulated by short-chain fatty acid (SCFA) ligands is involved in innate immunity and metabolism. GPR43 couples with Gα_i/o and Gα_q/11 heterotrimeric proteins and is capable of decreasing cyclic AMP and inducing Ca²⁺ flux. The GPR43 receptor has additionally been shown to bind β-arrestin 2 and inhibit inflammatory pathways, such as NF-κB. However, GPR43 shares the same ligands as GPR41, including acetate, propionate, and butyrate, and determination of its precise functions in association with endogenous ligands, such as SCFAs alone, therefore remains a considerable challenge. In this study, we generated novel synthetic agonists that display allosteric modulatory effects on GPR43 and downregulate NF-κB activity. In particular, the potency of compound 187 was significantly superior to that of pre-existing compounds in vitro. However, in the colitis model in vivo, compound 110 induced more potent attenuation of inflammation. These novel allosteric agonists of GPR43 clearly display anti-inflammatory potential, supporting their clinical utility as therapeutic drugs.