Journal of Clinical Immunology Research

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Opinion Article - Journal of Clinical Immunology Research (2023) Volume 6, Issue 1

Analysis of host and tumour variables in cancer immunology for individualised treatment.

Matthew Melero*

Department of Cancer Immunology, University of Amsterdam, Amsterdam, Netherlands

*Corresponding Author:
Matthew Melero
Department of Cancer Immunology
University of Amsterdam
Amsterdam, Netherlands
E-mail: matthew@nki.nl

Received: 05-Feb-2023, Manuscript No. AACIR-23-91971; Editor assigned: 08-Feb-2023, Pre QC No. AACIR-23-91971(PQ); Reviewed: 22-Feb-2023, QC No. AACIR-23-91971; Revised: 24-Feb-2023, Manuscript No. AACIR-23-91971(R); Published: 28-Feb-2023, DOI: 10.35841/aacir-6.1.135

Citation: Melero M. Analysis of host and tumour variables in cancer immunology for individualised treatment. J Clin Immunol. 2023;6(1):135

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Introduction

The most well-known application of cancer immunology, which uses the immune system as a cancer treatment, is cancer immunotherapy. Cancer immunology is an interdisciplinary area of biology that focuses on understanding the function of the immune system in the development and progression of cancer. Cancer immunosurveillance and immunoediting are based on I identifying targets for immune detection of human cancer (ii) and (iv) protection against tumour formation in animal systems [1].

The most well-known application of cancer immunology, where the immune system is used to treat cancer, is cancer immunotherapy. Cancer immunology is an interdisciplinary area of biology that examines the function of the immune system in the genesis and progression of cancer. Burnet and Thomas developed the concept of cancer immunosurveillance in 1957. They suggested that lymphocytes serve as sentinels, identifying and destroying continuously emerging, immature altered cells. Cancer immunosurveillance appears to be a crucial host defence mechanism that lowers cancer incidence rates by preventing carcinogenesis and maintaining constant cellular homeostasis. Moreover, it has been proposed that the primary role of immunosurveillance is to be a part of a broader process of cancer immunoediting [2].

Tumor-specific

Antigens known as Tumor-Specific Antigens (TSA) are found exclusively in tumour cells. TSAs can be made by oncoviruses such as the EBNA-1 protein of the EBV or the E6 and E7 proteins of the human papillomavirus, which are found in Burkitt's lymphoma cells and cervical cancer, respectively. Unusual byproducts of mutant oncogenes and anti-oncogenes, such as the Ras protein, are another illustration of TSAs.

The process of cancer immunoediting involves the immune system interacting with tumour cells. Elimination, equilibrium, and escape are its three stages. The "three Es" of cancer immunoediting are frequently referred to as these stages. Immunoediting involves both innate and adaptive immune systems. The immune response causes the tumour cells to be destroyed during the elimination phase, which suppresses the tumour. Certain tumour cells, however, may develop more mutations, alter their traits, and avoid the immune system. These cells may enter the equilibrium phase, in which the immune system does not recognise all tumour cells but the tumour does not enlarge at the same time [3].

Immunoediting has the effect of causing tumour cell clones to become more dominant over time when the immune system's identified cells are killed. Similar to Darwinian evolution, in this process, cells with pro-oncogenic or immunosuppressive mutations survive to pass on their mutations to daughter cells, which then have the potential to mutate and experience more selective pressure. As a result, the tumor's cells have a low immunogenicity and are difficult to eradicate. It has been established that cancer patients' immunotherapies are to blame for this phenomena.

It reasoned that by acting as a "bystander effect," the immune system could contribute to the elimination of chemotherapyresistant cancer cells. How the immune response is initiated against dying cancer cells, however, still requires a lot of study. According to experts in the area, necrotic cell death is truly immunogenic whereas apoptotic cell death is just marginally immunogenic. This may be due to the immune response being induced by the maturation of dendritic cells as a result of the inflammatory response being stimulated when cancer cells are eliminated via a necrotic cell death pathway [4].

An environment favourable to immunogenicity is created by anthracyclines. According to the researchers, this drug encourages antigen uptake and presentation by dendritic cells when killing cancer cells, triggering a T-cell response that can decrease tumours. Hence, the efficacy of immunotherapy depends on the activation of tumour-killing T-cells [5].

References

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  4. Dranoff G. Experimental mouse tumour models: what can be learnt about human cancer immunology?. Nat Rev Immunol. 2012;12(1):61-6.

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  5. Old LJ. Cancer immunology: the search for specificity—GHA Clowes Memorial lecture. J Cancer Res. 1981;41(2):361-75.

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