Unique expression of a small IL-32 protein in the Jurkat leukemic T cell line

Ko, Nayoung; Chang, Sung-Ho; Lee, Jun-Ho; Kim, Nam-Wook; Kim, Youngmi; Choi, Woojin; Choi, Jida; Bae, Sang Rak; Hong, Jaewoo; Jaekal, Jun; Azam, Tania; Her, Erk; Kim, Soohyun

doi:10.1016/j.cyto.2008.01.004

Cited by 15 publications

(12 citation statements)

References 16 publications

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“…Immunohistochemistry of normal lung tissue from patients with cancer and Ctrl patients showed that alveolar macrophages steadily expressed IL-32, whereas alveolar epithelium usually did not ( Figure 1A, a and b), except in the congested areas ( Figure 1A, c and d) close to the neoplastic lesions. The bronchial epithelium showed a scarce to moderate IL-32 expression ( Figure 1A, e and f), which was slightly less in the basal cell hyperplasia ( Figure 1A, g and h) and became scanty (ranging from weak to absent) in the atypical changes of the bronchial mucosa that may precede invasive SCC (20,21), such as SM ( Figure 1B, a and b), mild, moderate, and severe dysplasia ( Figure 1B, c and d), and SCIS ( Figure 1B, e and f, Table 1). By contrast, atypical changes of the alveolar walls, namely AAH, the putative precursor of AC (22,24,29), Table 1).…”

Section: Il-32 Expression In Premalignant Lung Lesionsmentioning

confidence: 95%

“…Its receptor is still unknown; even so, it is now recognized as proinflammatory mediator through its stimulation of TNF-a, IL-1b, IL-6, and IL-8 production, and its activation of the nuclear factor-kB (NFkB), and p38 mitogen-activated protein (MAP) kinase pathways (11,12). Although its function in a variety of inflammatory/ autoimmune and infective diseases is becoming clear (13)(14)(15)(16)(17)(18), its role in cancer has received little attention (19)(20)(21) and it is completely unexplored in lung cancer.…”

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confidence: 99%

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Expression of IL-32 in Human Lung Cancer Is Related to the Histotype and Metastatic Phenotype

Sorrentino

Carlo²

2009

Am J Respir Crit Care Med

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Section: Il-32 Expression In Premalignant Lung Lesionsmentioning

confidence: 95%

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confidence: 99%

Expression of IL-32 in Human Lung Cancer Is Related to the Histotype and Metastatic Phenotype

Sorrentino

Carlo²

2009

Am J Respir Crit Care Med

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“…The molecular weight of a distinctive IL-32 produced in Jurkat cells is smaller than IL-32a isoform. (15) However, the mRNA or amino acid sequence of this small IL-32 has not been identified yet. The result of FACS staining with …”

Section: Discussionmentioning

confidence: 99%

Interleukin-32 Gamma Specific Monoclonal Antibody and Developing IL-32 Specific ELISA

et al. 2010

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Cytokines are essential coordinators of defensive immune responses for resolving the invasion of pathogens such as bacteria, virus, and fungi. However, dysregulated cytokines are the main cause of various autoinflammatory immune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis. Interleukin-32 (IL-32) is a recently described cytokine and characterized as a proinflammatory cytokine. IL-32 stimulates monocytes and macrophages to induce important proinflammatory cytokines (IL-1β, IL-6, and TNFα) and chemokines (IL-8 and MIP-2) by activating the NF-κB and p38 mitogen-activated protein (MAP) kinase pathways. The biological activities of IL-32 are associated with epidemic pathogens, Mycobacterium tuberculosis, influenza A virus, and human immunodeficiency virus (HIV). IL-32 is transcribed as six alternative splice variants (α, β, γ, δ, ɛ, and ζ), with IL-32γ being the most active isoform. However, it is unclear which isoform is related to specific disease activities since there are no high quality antibodies available to measure circulating IL-32 in biological samples of patients. Therefore, we developed specific anti-human IL-32γ monoclonal antibodies from recombinant human IL-32γ, which was expressed in Escherichia coli. The IL-32γ specific monoclonal antibodies recognized IL-32 in cell culture supernatants and serum of IL-32γ transgenic mice. The newly developed IL-32γ monoclonal antibodies will be a useful tool to measure IL-32 level in serum samples of various inflammatory diseases. These monoclonal antibodies will be helpful in investigating the precise function of IL-32 in immune responses and in autoinflammatory diseases.

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“…The abundant expression of IL-32 in lungs of COPD patients (66) may indirectly indicate increased apoptosis because apoptosis is considered to be an important mechanism in the pathogenesis of COPD. However, apoptotic effects of IL-32 are not universally seen because IL-32 is constitutively expressed in various cancer cell lines or cancer tissues, suggesting that IL-32 may not only be antiapoptotic but may also be involved in the pathogenesis of some tumors (48,72,73).…”

Section: Discussionmentioning

confidence: 99%

IL-32 Is a Host Protective Cytokine against Mycobacterium tuberculosis in Differentiated THP-1 Human Macrophages

Bai

Kim

Azam

et al. 2010

The Journal of Immunology

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132

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Macrophages provide a first line of defense against Mycobacterium tuberculosis. However, in instances where macrophage activation for killing is suboptimal, M. tuberculosis is capable of surviving intracellularly. IL-32 is a recently described cytokine induced by M. tuberculosis in a variety of cell types including human monocytes and macrophages. In this study, we investigated the biological significance of IL-32 in an in vitro model of M. tuberculosis infection in differentiated THP-1 human macrophages in which IL-32 expression was silenced using stable expression of short hairpin RNA (shRNA). Inhibition of endogenous IL-32 production in THP-1 cells that express one of three distinct shRNA-IL-32 constructs significantly decreased M. tuberculosis induction of TNF-α by ∼60%, IL-1β by 30–60%, and IL-8 by 40–50% and concomitantly increased the number of cell-associated M. tuberculosis bacteria compared with THP-1 cells stably expressing a scrambled shRNA. In THP-1 cells infected with M. tuberculosis and stimulated with rIL-32, a greater level of apoptosis was observed compared with that with M. tuberculosis infection alone. Obversely, there was significant abrogation of apoptosis induced by M. tuberculosis and a concomitant decrease in caspase-3 activation in cells depleted of endogenous IL-32. rIL-32γ significantly reduced the number of viable intracellular M. tuberculosis bacteria, which was modestly but significantly abrogated with a caspase-3 inhibitor. We conclude that IL-32 plays a host defense role against M. tuberculosis in differentiated THP-1 human macrophages.

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Unique expression of a small IL-32 protein in the Jurkat leukemic T cell line

Cited by 15 publications

References 16 publications

Expression of IL-32 in Human Lung Cancer Is Related to the Histotype and Metastatic Phenotype

Expression of IL-32 in Human Lung Cancer Is Related to the Histotype and Metastatic Phenotype

Interleukin-32 Gamma Specific Monoclonal Antibody and Developing IL-32 Specific ELISA

IL-32 Is a Host Protective Cytokine against Mycobacterium tuberculosis in Differentiated THP-1 Human Macrophages

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