Immunological Approaches Towards Cancer and Inflammation: A Cross Talk

Abstract

The inflammation is the protective response of the body against various harmful stimuli; however, the aberrant and inappropriate activation tends to become harmful. The acute inflammatory response tends to resolved once the offending agent is subside but this acute response becomes chronic in nature when the body is unable to successfully neutralized the noxious stimuli. This chronic inflammatory microenvironment is associated with the release of various pro-inflammatory and oncogenic mediators such as nitric oxide (NO), cytokines [IL-1β, IL-2, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)], growth factor, and chemokines. These mediators make the inflammatory microenvironment more vulnerable toward tumorigenesis. The pro-inflammatory mediators released during the chronic inflammation tends to induce several molecular signaling cascades such as nuclear factor kappa B, MAPKinase, nuclear factor erythroid 2-related factor 2, phosphoinositide-3-kinase, Janus kinases/STAT, Wnt/B-catenin, and cyclic AMP response element binding protein. The immune system and its components have a pleiotropic effect on inflammation and cancer progression. Immune components such as T cells, natural killer cells, macrophages, and neutrophils either inhibit or enhance tumor initiation depending on the type of tumor and immune cells involved. Tumor-associated macrophages and tumor-associated neutrophils are pro-tumorigenic cells highly prevalent in inflammation-mediated tumors. Similarly, presence of T regulatory (Treg) cells in an inflammatory and tumor setting suppresses the immune system, thus paving the way for oncogenesis. However, Treg cells also inhibit autoimmune inflammation. By contrast, cytotoxic T cells and T helper cells confer antitumor immunity and are associated with better prognosis in patients with cancer. Cytotoxic T cells inflict a direct cytotoxic effect on cells expressing oncogenic markers. Currently, several anti-inflammatory and antitumor therapies are under trials in which these immune cells are exploited. Adoptive cell transfer composed of tumor-infiltrating lymphocytes has been tried for the treatment of tumors after their ex vivo expansion. Mediators released by cells in a tumorigenic and inflammatory microenvironment cross talk with nearby cells, either promoting or inhibiting inflammation and cancer. Recently, several cytokine-based therapies are either being developed or are under trial to treat such types of manifestations. Monoclonal antibodies directed against TNF-α, VEGF, and IL-6 has shown promising results to ameliorate inflammation and cancer, while direct administration of IL-2 has been shown to cause tumor regression.

Pathogenic role of exosomes and microRNAs in HPV‐mediated inflammation and cervical cancer: A review

“…Chronic inflammation takes place for two main reasons: ( i ) the host is unable to eliminate the original stimulus or ( ii ) the host cannot carry out the resolution of inflammation program . Chronic inflammation involves progressive changes in several kinds of inflammatory cells and can participate in the causation of chronic diseases, such as cardiovascular, arthritis, diabetes, neurological diseases and cancer …”

“…32 Chronic inflammation involves progressive changes in several kinds of inflammatory cells and can participate in the causation of chronic diseases, such as cardiovascular, arthritis, diabetes, neurological diseases and cancer. 33 Researchers have suggested that there is a relationship between inflammation and cancer, but this suggestion is not a thoroughly novel idea, because Rudolf Virchow (1863) demonstrated that inflammation and chronic irritation could lead to cancers. 34 Nowadays, inflammation is accepted as a significant cancer hallmark ( Fig.…”

Cytokine rs361525, rs1800750, rs1800629, rs1800896, rs1800872, rs1800795, rs1800470, and rs2430561 SNPs in relation with prognostic factors in acute myeloid leukemia

“…Cytokines (interleukins [ILs], growth factors, interferons, etc) play an important role in regulating the inflammatory response, and chronic inflammation and are involved in cancer development . Chronic inflammation is associated with the release of various mediators (pro‐inflammatory and oncogenic ones), such as reactive nitrogen oxygen species, inflammatory cytokines (IL‐1β, IL‐2, IL‐6, and tumor necrosis factor alpha [TNF‐α]), growth factors, and chemokines …”

“…1,2 Cytokines (interleukins [ILs], growth factors, interferons, etc) play an important role in regulating the inflammatory response, and chronic inflammation and are involved in cancer development. 3,4 Chronic inflammation is associated with the release of various mediators (pro-inflammatory and oncogenic ones), such as reactive nitrogen oxygen species, inflammatory cytokines (IL-1β, IL-2, IL-6, and tumor necrosis factor alpha [TNF-α]), growth factors, and chemokines. 4 Based on their inflammatory activity, cytokines are divided into pro-inflammatory (IL-6, IL-17, IL-18, TNF-α, interferon gamma [IFN-γ], etc) 5 and anti-inflammatory (Il-4, IL-10, IL-13, etc) ones, whereas several cytokines have a dual role (IL-10, IL-22, TGF-β1).…”

“…3,4 Chronic inflammation is associated with the release of various mediators (pro-inflammatory and oncogenic ones), such as reactive nitrogen oxygen species, inflammatory cytokines (IL-1β, IL-2, IL-6, and tumor necrosis factor alpha [TNF-α]), growth factors, and chemokines. 4 Based on their inflammatory activity, cytokines are divided into pro-inflammatory (IL-6, IL-17, IL-18, TNF-α, interferon gamma [IFN-γ], etc) 5 and anti-inflammatory (Il-4, IL-10, IL-13, etc) ones, whereas several cytokines have a dual role (IL-10, IL-22, TGF-β1). 6 Interleukin-10, an anti-inflammatory cytokine, has dual functions, being both immune-suppressive (tumor-inhibiting) and immune-stimulating (tumor-promoting), and may, therefore, influence tumor susceptibility and development.…”