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IL32
IL32 Full Name
Interleukin 32
IL32 Introduction
In contrast to other members of the interleukin family, IL-32 lacks a classical signal peptide sequence, and amino acid sequence homology with other cytokines is low. The IL-32 gene has multiple exons and maps to human chromosome 16. Alternative splicing of IL-32 pre-mRNA can lead to the generation of different splice isoforms including IL-32α, β, γ, δ, ε, ζ, η, θ, and ι. The shortest isoform, IL-32α, is the most abundant intracellular isoform; however, secreted IL-32β and IL-32γ proteins are the most studied and are the most biologically active isoforms of IL-32. Different isoforms of IL-32 have varying functions. IL-32γ is believed to be the most pro-inflammatory, while other isoforms have distinct and/or opposing functions.
Figure 1. Schematic Representation of IL32β, IL32γ and IL32δ protein structure. (Source: Gautam A, et al. 2021)
IL-32 is primarily produced by immune cells such as activated T lymphocytes, NK cells, monocytes, macrophages, but can also be expressed in non-immune cells, including epithelial cells, fibroblasts, and endothelial cells in response to specific stimuli. IL-32 is generally believed to be a pleiotropic pro-inflammatory cytokine that is involved in immune regulation and inflammation. It primarily promotes and maintains inflammation and can also induce the production of a number of other key inflammatory mediators. Extracellularly secreted IL-32 acts on target cells and can activate a variety of intracellular signaling pathways, the most notable of which are NF-κB and p38 MAPK signaling pathways. This in turn upregulates the gene expression of a series of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 and chemokines, which further amplifies the inflammatory response by positive feedback. In addition to its classical pro-inflammatory function, the other functions of IL-32 are also complicated. Recent studies have shown that IL-32 is also involved in the processes of apoptosis, cell differentiation, angiogenesis, and many other cellular functions. Moreover, IL-32 is also essential for host antiviral immunity. It can be induced by viruses and can inhibit viral replication in various ways. IL-32 also exhibits antiviral activity in models of influenza virus and HIV infection.
Dysregulated IL-32 expression is closely associated with human diseases, particularly autoimmune diseases, chronic inflammatory diseases, infectious diseases and cancer. In rheumatoid arthritis, IL-32 was found as one of the major pathogenic factors. Increased IL-32 levels could be detected in RA synovial tissue and synovial fluid, and IL-32 expression in PBMCs from RA patients showed a good correlation with disease activity and severity. In affected joints, IL-32 induced inflammatory cascades, osteoclast differentiation and destruction of articular cartilage and bone. Similarly to RA, increased IL-32 expression was also observed in other Th1-mediated immune diseases, such as psoriasis and IBD, and IL-32 plays a role in the localized inflammatory damage in the skin and intestinal mucosa. In viral infections, the roles of IL-32 are more complicated. On one hand, as the host defense, increased IL-32 expression functions to suppress viral replication and might play a potential role in restraining viral load in HIV-1 infection. On the other hand, excessive IL-32 response might amplify the cytokine storm and tissue injury induced by viral infection. In cancer research, IL-32 functions as a "double-edged sword". In some types of cancer, including gastric cancer and liver cancer, IL-32 stimulates cancer cell migration, invasion, and angiogenesis, and accelerates tumor progression. However, IL-32-induced apoptosis was also discovered in various cancer cells, which presents an opposite, anti-tumor effect of IL-32.
Alternate Names for IL32
IL32; Interleukin 32; NK4; TAIF; TAIFa; TAIFb; TAIFc; TAIFd; IL-32beta; IL-32alpha; IL-32delta; IL-32gamma
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