Immunology of IL-12: An update on functional activities and implications for disease

Ullrich, Karen A-M; Schulze, Lisa Lou; Paap, Eva-Maria; Müller, Tanja M.; Zundler, Sebastian

doi:10.17179/excli2020-3104

Cited by 32 publications

(15 citation statements)

References 214 publications

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“…IL-12p70 plays an essential role as the principal component of IL-12 that exerts biological effects on numerous autoimmune diseases or chronic diseases, like multiple sclerosis, diabetes, and psoriasis. 34 In the present research, no noticeable augmentation of IL-12p70 was found in aSAH, which might be explained by the fact that IL-12 does not play an important role in diseases with acute onset and rapid progression. In addition to IL-10, the cytokines associated with disease severity were IL-2, IL-6, IL-8, and IFN-α.…”

Section: Discussioncontrasting

confidence: 70%

Clinical Value of Inflammatory Cytokines in Patients with Aneurysmal Subarachnoid Hemorrhage

Luo¹,

Yao²,

Bi³

et al. 2022

CIA

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Section: Discussioncontrasting

confidence: 70%

Clinical Value of Inflammatory Cytokines in Patients with Aneurysmal Subarachnoid Hemorrhage

Luo¹,

Yao²,

Bi³

et al. 2022

CIA

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“…In fact, treatment with IL-12+IL-18 of healthy HFs selectively enriches IFN-γ-inducible genes and promotes the release of IFN-γ into the medium and thus HF-IP collapse. These responses were abrogated by co-administration of a selective TYK2 inhibitor (Edelkamp et al, 2021), which confirms a key role of IL-12, whose receptor utilizes a TYK2 and Janus kinase 2 pair for downstream signal transduction (Ullrich et al, 2020; Krueger et al, 2022), These preliminary findings suggest that IL-12 is a key effector cytokine in promoting pathogenic IFN-γ secretion and HF-IP collapse. Given that ILC1 are IFN-γ producing cells (Nabekura et al, 2021b; Resende et al, 2017; Quintino-de-Carvalho et al, 2022), our data therefore encourage one to dissect, next, the exact role of IL-12/IL-12R-mediated signaling in activating, attracting and/or expanding ILC1-like cells and in stimulating their IFN-γ secretion in the early stages of human AA pathogenesis.…”

Section: Discussionmentioning

confidence: 84%

Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata

Britva

Keren

Bertolini

et al. 2022

Preprint

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Here, we have explored the involvement of innate lymphoid cells-type 1 (ILC1) in the pathogenesis of alopecia areata (AA), because we found them to be significantly increased around lesional and non-lesional HFs of AA patients. To further explore these unexpected findings, we first co-cultured autologous circulating ILC1-like cells (ILC1lc) with healthy, but stressed, organ-cultured human scalp hair follicles (HFs). ILClc induced all hallmarks of AA ex vivo: they significantly promoted premature, apoptosis-driven HF regression (catagen), HF cytotoxicity/dystrophy and most important for AA pathogenesis, collapse of the HFs physiological immune privilege. NKG2D-blocking or IFNγ-neutralizing antibodies antagonized this. In vivo, intradermal injection of autologous activated, NKG2D+/IFNγ-secreting ILC1lc into healthy human scalp skin xenotransplanted onto SCID/beige mice sufficed to rapidly induce characteristic AA lesions. This provides the first evidence that ILC1lc suffice to induce AA in previously healthy human HFs ex vivo and in vivo, and further questions the conventional wisdom that AA is always an autoantigen-dependent, CD8+ T cell-driven autoimmune disease.

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“…Clinical studies have found that serum IL-12 in patients with HBV-ACLF is significantly elevated (approximately 2 times) compared with severe chronic hepatitis B, moderate chronic hepatitis B, and healthy controls [ 57 , 58 ]. IL-12 induces IL-21 through transcription factors STAT1, STAT3, STAT4, and STAT5 [ 59 ] and enhances T follicular helper (Tfh) cells differentiation [ 60 ]. Upregulated Tfh cells and IL-21 are closely related to the severity and improvement of HBV-ACLF, and increased IL-12 may be related to the occurrence of ACLF.…”

Section: Interleukin-12mentioning

confidence: 99%

Serum Interleukins as Potential Prognostic Biomarkers in HBV-Related Acute-on-Chronic Liver Failure

Zhang

Gou

et al. 2022

Mediators of Inflammation

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Hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is relatively common in China and has complex pathogenesis, difficult clinical treatment, and poor prognosis. Immune status is an important factor affecting ACLF prognosis. Interleukins are a family of secreted lymphocyte factors that interact with a host of cell types including immune cells. These signaling molecules play important roles in transmitting information; regulating immune cells; mediating the activation, proliferation, and differentiation of T and B cells; and modulating inflammatory responses. Many studies have investigated the correlation between interleukin expression and the prognosis of HBV-ACLF. This review focuses on the potential use of interleukins as prognostic biomarkers in HBV-ACLF. References were mainly identified through PubMed and CNKI search, including relevant studies published until December 2021. We have summarized reports of several promising diagnostic interleukin biomarkers that predict susceptibility to HBV-ACLF. The use of biomarkers to understand early prognosis can help devise different therapeutic measures and improve patient survival. Ongoing research on prognostic biomarkers of HBV-ACLF is promising, and future preclinical and clinical studies are warranted.

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Immunology of IL-12: An update on functional activities and implications for disease

Cited by 32 publications

References 214 publications

Clinical Value of Inflammatory Cytokines in Patients with Aneurysmal Subarachnoid Hemorrhage

Clinical Value of Inflammatory Cytokines in Patients with Aneurysmal Subarachnoid Hemorrhage

Involvement of ILC1-like innate lymphocytes in human autoimmunity, lessons from alopecia areata

Serum Interleukins as Potential Prognostic Biomarkers in HBV-Related Acute-on-Chronic Liver Failure

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