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Role of Nanoparticles in Cancer Immunotherapy
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
Though tumor immunosurveillance hypothesis emphasizes the ability of immune cells to recognize and eliminate cancer cells; however, many patients develop cancer even in the presence of an apparently normal immune system. This indicates that tumor cells are able to escape immune surveillance. To avoid attack from the immune system, tumor cells develop different strategies to escape immune surveillance. Cancer immune evasion is a major limitation for developing an effective therapeutic approach to treat cancer. To have a successful anticancer immune response, the tumor-immunity cycle should be circulated uninterrupted [24]. Blockade at any step in the pathway leads to unresponsiveness. Cancer cells develop different strategies to interrupt the tumor-immunity cycle. In below sections, we review different escape mechanisms employed by cancer cells.
Introduction to Infection, Resistance, and Immunity
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Some pathogens are capable of survival and replication in the absence of host species, but other pathogens have an absolute requirement for a host. Survival of the latter organisms requires both host availability and evasion of immune elimination at least until transmission to a new host. Host immune systems and pathogen immune evasion strategies are products of the coevolution of hosts and pathogens and development of both systems is an ongoing process.
Herpesvirus microRNAs for Use in Gene Therapy Immune-Evasion Strategies
Published in Yashwant Pathak, Gene Delivery, 2022
Vineet Mahajan, Shruti Saptarshi, Yashwant Pathak
Antibodies produced by non-self-antigens may compromise the recipient’s immune system cell survival after grafting. Immunosuppressive drugs may be required for the rest of the recipient’s life when receiving the graft.3 In addition to immune-evasion molecules, another approach that could reduce graft rejection is using DNA mutations. It is possible to subvert an immune response by expressing such molecules in the tissues of a graft. A virus in particular is extremely adept at manipulating the immune response of its hosts.1 The Herpes Simplex Virus (HSV) genome size and ability to be latent in neuronal cells make it unique for such gene delivery in the designated system, such as the nervous system, regarding its large genome size and for delivery of genes.1 The Herpesviridae family provides a reasonable proof of concept for this, since they have the ability to establish latency in the infected host and to persist for life. Many viral proteins involved in immune evasion have been characterized; however, the Herpesviridae also encode a large and diverse range number of viral microRNAs (miRNAs). Immune evasion is linked to some of them. Researchers have shown that several miRNAs inhibit the host’s immune system from destroying infected cells.4,5 In this chapter, miRNAs from some common herpesviruses that modulate immune responses will be discussed, culminating with a discussion of their potential application in non-immune generating cell therapy.
Immune-based therapies in diffuse large B-cell lymphoma
Published in Expert Opinion on Investigational Drugs, 2023
Dustin McCurry, Christopher R. Flowers, Casey Bermack
In addition to direct cytotoxic activity, CAR T-cells additionally exert indirect therapeutic effects via recruitment, activation, and expansion of endogenous host immune responses. In the absence of complete tumor cell eradication, CAR T-cells exert selective pressure for tumors to evolve away from CAR recognition. Thus, durable CAR T-cell mediated responses likely rely upon a combination of maximal initial cytotoxic activity to eradicate disease, in conjunction with education of the host immune system to recognize a broader array of tumor antigens/epitopes to decrease the chances of complete evasion of the immune system. Additional interrogation of host immune contributions to anti-tumor activity after CAR T-cells will inform strategies to promote the durability of responses and to counter tumor immune evasion.
Host factors subverted by Mycobacterium tuberculosis: Potential targets for host directed therapy
Published in International Reviews of Immunology, 2023
Rashi Kalra, Drishti Tiwari, Hedwin Kitdorlang Dkhar, Ella Bhagyaraj, Rakesh Kumar, Anshu Bhardwaj, Pawan Gupta
An alternate theory of disease causation as proposed by Pierre Jacques Antoine Bechamp (1816–1908), advocates that the human body’s “internal milieu” or “terrain” is responsible for development of disease post infection [187]. After several years of research, it is now well established that a wide range of “host factors” modulate the body’s “internal milieu” and influence disease susceptibility, treatment response and mortality rates. Therefore, host immunity is of paramount importance. In order to be a successful host, one should be able to tolerate damage caused by the pathogen and the immune system along with efficient pathogen clearance. This ability of tolerance is described as “host resilience” and is a relatively unexplored research niche [188,189]. The available treatment options predominantly target pathogen clearance; hence are antimicrobial in nature. However, proper attention has not been given to molecules that enhance host tolerance and target pathogens in a “non-microbial” fashion. Given this, there arises a need for understanding the host factors behind resilience for tailoring appropriate treatment options. It is believed that host molecules aiding M. tuberculosis during pathogenesis might be one of the factors responsible for this tolerance. Thus, detailed identification of the host molecules subverted by the pathogen for immune evasion is cardinal for pathogen clearance as well as for boosting the immune system in times of pandemics, such as the recent coronavirus (COVID-19). In the coming years, an investment of scientific efforts in this discipline will be required and is anticipated.
Yin and yang of immunological memory in controlling infections: Overriding self defence mechanisms
Published in International Reviews of Immunology, 2022
Roshan Kumar Roy, Rakhi Yadav, Aklank Jain, Vishwas Tripathi, Manju Jain, Sandhya Singh, Hridayesh Prakash
Thus, innate cells, effector lymphocytes and memory lymphoid cells work in concert to destroy large variety of pathogens by producing and maintaining memory network which helps host to combat re-infection with much amplified immune-resistance in a pathogen specific manner as represented in Figure 1. However, the clinical spectrum of infectious diseases suggests immune evasion strategies employed by pathogen to weaken the effector and memory response. The phenomenon is specifically relevant for latent infections where the pathogen is able to successfully subvert the host recall mechanism to clear the infection. Thus, understanding B and T cell immunological memory in context of latent infection with bacterial and viral pathogens is paramount for designing effective immune therapeutics. In view of this, we have discussed in detail about the role and regulation of immunological memory for managing various infections. Besides this, we have also discussed about challenges and possible interventional approaches/vaccine strategies for enhancing memory response mechanisms with potential to contribute towards the management of these infections