IL-32γ induces chemotaxis of activated T cells via dendritic cell-derived CCL5

Son, Mi Hye; Jung, M.; Choi, Soo In; Cho, Daeho; Kim, Tae Sung

doi:10.1016/j.bbrc.2014.05.052

Cited by 20 publications

(19 citation statements)

References 19 publications

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“…6 In turn, IL-32 increases the production of the cytokines tumour necrosis factor (TNF)-a, IL-1b and IL-6, 6,9 and also of the chemokines IL-8, CCL2, CCL4 and CCL5. 6,10,11 Moreover, IL-32 was shown to upregulate the adhesion molecules ICAM-1 and sVCAM-1 10,12 and the antimicrobial peptide (AMP) cathelicidin. 13 In addition to its proinflammatory features, IL-32 negatively impacts on cancer cell growth 14 and has a protective role in viral and bacterial infections.…”

Section: What Is the Translational Message?mentioning

confidence: 99%

Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa

et al. 2017

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Section: What Is the Translational Message?mentioning

confidence: 99%

Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa

et al. 2017

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“…In murine bone marrow-derived DCs, rhuIL-32g activates the PLC/JNK/NF-kB pathway to induce IL-12 and IL-6 production, thus contributing to Th1 and Th17 profiles, respectively [50]. In addition, murine DCs treated with rhuIL-32g produce CCL chemokines, especially CCL5, to induce chemotaxis of CD4 + or CD8 + T lymphocytes [52]. Furthermore, IL-32g controls not only innate immune responses but also drives acquired immunity and increases the recruitment of T cells.…”

Section: General Properties Of Il-32mentioning

confidence: 99%

Interleukin 32: a novel player in the control of infectious diseases

Ribeiro‐Dias

Gomes

Silva

et al. 2016

Journal of Leukocyte Biology

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Interleukin 32 (IL-32) is a proinflammatory cytokine, expressed as 9 distinct isoforms. The most active isoform is the predominantly intracellular-functioning IL-32γ. Involvement of IL-32 in infectious diseases is increasingly being appreciated. Production of IL-32 promotes pathways that serve to control bacterial infection, especially those caused by mycobacteria. A similar role for this cytokine is observed in the cellular response to viral infections. In addition to its protective effects against microorganisms, IL-32 is involved in immunopathogenesis of some infectious diseases. In parasitic diseases, it has been demonstrated that this cytokine is induced by Leishmania infection. In this review, we summarize the present data on the role of IL-32 in infectious diseases, highlighting this cytokine as new target for control of infections.

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“…IL-32 plays a critical role in the differentiation and activation of macrophages [ 106 ]. Furthermore, IL-32 cooperates with TNFα and IL-17 in facilitating increased production of other pro-inflammatory cytokines and chemokines leading to chronic inflammation and osteoclastic bone erosion in RA [ 107 ]. IL-32 induces the production of IL-17 in CD4 + T cells, and reciprocally IL-17 affects the expression of IL-32 in fibroblasts-like synoviocytes (FLSs) of RA patients [ 108 ].…”

Section: The Relatively Newer Cytokines (Il-32 Il-34 and Il-35) Amentioning

confidence: 99%

Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy

Venkatesha

Dudics

Acharya

et al. 2014

IJMS

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Cytokines are the key mediators of inflammation in the course of autoimmune arthritis and other immune-mediated diseases. Uncontrolled production of the pro-inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and IL-17 can promote autoimmune pathology, whereas anti-inflammatory cytokines including IL-4, IL-10, and IL-27 can help control inflammation and tissue damage. The pro-inflammatory cytokines are the prime targets of the strategies to control rheumatoid arthritis (RA). For example, the neutralization of TNFα, either by engineered anti-cytokine antibodies or by soluble cytokine receptors as decoys, has proven successful in the treatment of RA. The activity of pro-inflammatory cytokines can also be downregulated either by using specific siRNA to inhibit the expression of a particular cytokine or by using small molecule inhibitors of cytokine signaling. Furthermore, the use of anti-inflammatory cytokines or cytokine antagonists delivered via gene therapy has proven to be an effective approach to regulate autoimmunity. Unexpectedly, under certain conditions, TNFα, IFN-γ, and few other cytokines can display anti-inflammatory activities. Increasing awareness of this phenomenon might help develop appropriate regimens to harness or avoid this effect. Furthermore, the relatively newer cytokines such as IL-32, IL-34 and IL-35 are being investigated for their potential role in the pathogenesis and treatment of arthritis.

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IL-32γ induces chemotaxis of activated T cells via dendritic cell-derived CCL5

Cited by 20 publications

References 19 publications

Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa

Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa

Interleukin 32: a novel player in the control of infectious diseases

Cytokine-Modulating Strategies and Newer Cytokine Targets for Arthritis Therapy

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