Cancer remission due to immune impairment: A review report

R. R. Elamathi*

*Correspondence:
R. R. Elamathi,
dr.elamathi96@gmail.com

Received: 05 June 2023; Accepted: 13 June 2023; Published: 12 July 2023.

Keywords: cancer, immune impairment, remission, immunotherapy, spontaneous remission, tumor microenvironment, immune suppression, immune system, cancer treatment, immunodeficiency disorders

Introduction

Immune develops in reaction to the presence of a cancerous tumor as it grows to a certain size, rather than through immunological sensitization. This is most likely due to the tumor’s slow growth, giving the immune system more time to acclimate to the new environment. Some immune system components generate “adaptive immunity” in response to a growing malignant growth, while other immune system components aim to prevent cancerous growth from developing. The immune system’s protective arm is often responsible for assuring the advancement of malignant growth. Because of the immunological tolerance, the immune system may misidentify the malignant growth as a component of the body with which it is already acquainted, adding to the protective impact. Immunological paralysis may be caused by a severe infection or a tumor mass that is excessively large. Both of these variables may lead immune system components entrusted with safeguarding the body against malignant growths to become overburdened and shut down. Immunological paralysis may be caused by any of these reasons. At this stage, several immune system components are no longer capable of providing any protection against the creation of malignant tumors. At this point, it is projected that the malignant disease will go into remission after a simple acute inflammation, followed by remission. This is because the inflammation would be followed by remission.

A complete and systematic evaluation of the accounts of spontaneous remission of cancer suggests, in at least two areas, that the rejection of the malignant development by the immune system may be related to the temporary loss of the immune system defending the malignant growth. This conclusion was obtained after analyzing stories of spontaneous cancer remission. When examining the cases of cancer patients who had spontaneous remission, one reaches this conclusion. On the basis of the facts supplied in the reports, one may arrive at the following conclusion after considerable reflection: (1) a very severe kind of illness and (2) an excessively large number of distinct cancer forms.

Immune paralysis is a possible side effect of a severe infection or sepsis (1, 2), and there have been reported examples of cancer remission after a severe sickness. Moreover, when the tumor burden is unusually high, such as when people live with a large tumor burden, the immune system becomes paralyzed because it is unable to appropriately combat the massive malignant development. This happens when a person has a substantial tumor burden. As a consequence, the immune system is rendered paralyzed. It has been shown that when the volume of the immune response increases in contrast to the volume of the tumor, the immune response becomes less effective. There have been reports of cancer patients, in both human and animal, experiencing spontaneous remissions after the tumor had grown to huge proportions (3). The cancer had already progressed to an advanced level in these patients.

Discussion

The immune system is made up of many separate subsystems, each with its own distinguishing nomenclature. They are the innate and adaptive immune systems, respectively. The two subcategories of innate immunity are cellular immunity and humoral immunity. Platelets and natural killer (NK) cells are two kinds of cells that exhibit cellular immunity (complement and cytokines). NK cells, which are part of an individual’s innate immune system, have the ability to eliminate cancer cells. Although the innate and adaptive immune systems are continually sharing information, only one kind of immunity may be active in response to a stimulus at any one moment. It is not conceivable to activate both the innate and adaptive immune systems in response to the same stimuli. When anything like this occurs, neither kind of immunity is activated.

The natural immunity that exists inside the body is the body’s first line of defense against sickness. It may identify unknown compounds and cells in the body that are damaged or not functioning correctly owing to a malfunction (neoplasm). The immune system’s innate defenses communicate information with the immune system’s adaptive defenses, allowing the adaptive defenses to clear potentially hazardous chemicals from the body.

Tumorigenesis develops slowly, causing tolerance rather than sensitivity and evading detection by innate immunity. As tolerance is established, adaptive immunity becomes protective of malignant development while suppressing innate immunity from starting an immunological attack. Innate and adaptive immunity cannot both be activated in the same instance in response to the same stimuli.

If there is an acute inflammatory reaction, platelets are in charge of activating NK cells. NK cells play a crucial role in infection resistance. NK cells are ultimately responsible for the eradication of malignant cells (innate immunity). Platelets, on the contrary, hinder NK cells’ capacity to eradicate cancerous cells at any stage of the disease’s progression. This occurs as a result of platelets clogging blood arteries and causing bleeding. Immunoglobulin is another kind of chemical that has the ability to strengthen the immune system. Immunoglobulins are incapable of eliciting an efficient immune response in the body in response to tumor growth. There is a potential that adaptive immunity influences the activity of both innate and humoral immunity. This would be the case if adaptive immunity was active.

When the tumor’s bulk becomes larger, an immune activity that combats malignant growth becomes less effective. These findings may be interpreted in a variety of ways, one of which is that “a decrease in immune activity against malignant growth correlates with a decrease in immunological protection against malignant development.” To put it another way, the immune system will eventually quit battling cancerous growth, at which point it will be able to remove the disease. This occurs when the immune system no longer protects the tumor in the issue.

Suggested experimental treatment

(1) When the host progressively rids itself of the antigen, it continually creates an acute inflammation beneath the skin so that as soon as adoptive immunity gets activated, it will come into contact with the acute inflammatory reaction (prior to adoptive immunity suppressing innate immunity). It is possible that this will cause the immunological state to change from one of tumor protection and rejection to one of tumor rejection. Owing to the fact that the initial inflammatory response might provide a message to the adaptive immune system indicating that the malignant development is not native, the severity of the acute inflammation is inversely correlated with the likelihood of remission.

(2) It is possible that a mild dosage of corticosteroids (like dexamethasone) might be beneficial.

(3) It is possible that the impact might be enhanced by administering a modest and low dosage of aspirin 1 h before triggering an acute inflammatory reaction. Due to the danger of life-threatening internal bleeding, extreme caution should be used. If the patient does not have a disease that would prevent the use of aspirin, it is possible to give them the medication. As the half-life of aspirin is so lengthy, a second dosage may be given after 2 days, provided there are no adverse drug interactions and the patient does not have a condition that would make it unsafe for them to take the medication.

(4) Causing immune system paralysis by exposing it to an excessive amount of antigen.

(5) Inducing a severe inflammatory response under the skin after having already produced immunological paralysis (as long as immune paralysis is present, possibly adaptive immunity may not suppress innate immunity).

(6) Injecting plasma-rich platelets into the area where the acute inflammation is located may have an amplifying impact.

(7) There is a possibility that temporarily inhibiting cellular immunity will have an additive impact. There is a possibility that drugs that inhibit graft rejection will be employed. Because of the potentially life-threatening impact that these medications might have, they should be used with extreme caution.

(8) A skin test for tuberculosis may be performed. When delayed-type hypersensitivity has been eliminated entirely, it is reasonable to conclude that adaptive immunity has been temporarily reduced.

Caution

Mandatory Attendance at a Medical Facility: it is possible that the patient’s condition will prevent them from receiving a non-live vaccination. There is no evidence to indicate that the experimental therapy that has been recommended would be successful. It is predicated on a concept that proposes an immune mechanism as the cause of cancer going into spontaneous remission after acute infections. As a result, I would recommend experimental therapy for those who have cancer.

Summary

It has been hypothesized that a brief and temporary immunological paralysis (the suppression of adaptive immunity), followed by acute inflammation, may perhaps be followed by the remission of the malignant condition. This idea has been supported by a number of studies. This is an event that has the possibility of taking place. The immune system is not operating correctly because it is simultaneously working to prevent the development of cancer while also attempting to defend itself against it. It is hypothesized that if the immune system stops defending or rejecting the malignant growth, it will realign itself, which will lead to the immune system’s eradication of the malignant growth. This is a consequence of the immune system’s failure to protect or reject malignant growth. This is the result of the immune system no longer protecting or rejecting the growth as it should have been doing.

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