Yin and yang of interleukin-17 in host immunity to infection

Das, Shibali; Khader, Shabaana A.

doi:10.12688/f1000research.10862.1

Cited by 65 publications

(54 citation statements)

References 177 publications

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“…In contrast, later IL-17 neutralization did not result in severe disease progression and only slightly increased HN878 burden at the time of harvest (Figure 2, A-C). While Th17 cells are a major source of IL-17 in HN878 infection, γδ T cells can also produce IL-17 early after HN878 infection (22). Consistent with these findings, γδ T cells were the major lymphocytic source of IL-17 in HN878 lungs despite accumulation of CD4 + and CD8 + T cells producing IL-17 in the lungs of HN878-infected mice ( Figure 2D).…”

Section: Il-17 Limits Hif1α Expression In Vitro While Il-17 Neutralisupporting

confidence: 78%

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Interleukin-17 limits hypoxia-inducible factor 1α and development of hypoxic granulomas during tuberculosis

Domingo-Gonzalez¹,

Das²,

Griffiths³

et al. 2017

JCI Insight

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Section: Il-17 Limits Hif1α Expression In Vitro While Il-17 Neutralisupporting

confidence: 78%

“…IL-17 has a well-documented role in the induction of chemokines that mediate neutrophil recruitment for pathogen control (22). Thus, we determined whether IL-17 neutralization affected neutrophil accumulation in HN878-infected lungs.…”

Section: Il-17 Neutralization Leads To Mdsc Accumulation and Decreasementioning

confidence: 99%

Interleukin-17 limits hypoxia-inducible factor 1α and development of hypoxic granulomas during tuberculosis

Domingo-Gonzalez¹,

Das²,

Griffiths³

et al. 2017

JCI Insight

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“…Th17 cells are best known for their roles in immunosurveillance of mucosal barrier surfaces and in many autoimmune and inflammatory diseases. The role of IL-17 during intracellular and viral infections remains unclear, because there is evidence both for protective and pathological roles [26,27]. Finally, we observed that a reduced frequency of CD8 and CD4 T cells producing TNFα at baseline is associated with protection from mortality upon virus infections ( Figure 3C and F).…”

Section: Associated With Increased Risk Of Death After Virus Infectionmentioning

confidence: 77%

Immune predictors of mortality following RNA virus infection

Graham

Swarts

Menachery

et al. 2019

The Journal of Infectious Diseases

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Background Virus infections result in a range of clinical outcomes for the host, from asymptomatic to severe or even lethal disease. Despite global efforts to prevent and treat virus infections to limit morbidity and mortality, the continued emergence and re-emergence of new outbreaks as well as common infections such as influenza persist as a health threat. Challenges to the prevention of severe disease after virus infection include both a paucity of protective vaccines, as well as the early identification of individuals with the highest risk that may require supportive treatment. Methods We completed a screen of mice from the Collaborative Cross (CC) that we infected with influenza, SARS-coronavirus, and West Nile virus. Results CC mice exhibited a range of disease manifestations upon infections, and we used this natural variation to identify strains with mortality following infection and strains exhibiting no mortality. We then used comprehensive pre-infection immunophenotyping to identify global baseline immune correlates of protection from mortality to virus infection. Conclusions These data suggest that immune phenotypes might be leveraged to identify humans at highest risk of adverse clinical outcomes upon infection, who may most benefit from intensive clinical interventions, in addition to providing insight for rational vaccine design.

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“…To date, no cases of reactivation of latent tuberculosis (TB) infection (LTBI) were observed. 17 However, reports that IL-17A-producing γδT cells and CD4 + T cells might have protective or pathologic roles during different phases of Mycobacterium tuberculosis infection 15,16,[18][19][20][21][22] emphasize the need to further explore the role of IL-17A in this context.…”

mentioning

confidence: 99%

Inhibition of IL‐17A by secukinumab shows no evidence of increased Mycobacterium tuberculosis infections

et al. 2017

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Secukinumab, a fully human monoclonal antibody that selectively neutralizes interleukin-17A (IL-17A), has been shown to have significant efficacy in the treatment of moderate to severe psoriasis, psoriatic arthritis and ankylosing spondylitis. Blocking critical mediators of immunity may carry a risk of increased opportunistic infections. Here we present clinical and in vitro findings examining the effect of secukinumab on Mycobacterium tuberculosis infection. We re-assessed the effect of secukinumab on the incidence of acute tuberculosis (TB) and reactivation of latent TB infection (LTBI) in pooled safety data from five randomized, double-blind, placebo-controlled, phase 3 clinical trials in subjects with moderate to severe plaque psoriasis. No cases of TB were observed after 1 year. Importantly, in subjects with a history of pulmonary TB (but negative for interferon-γ release and receiving no anti-TB medication) or positive for latent TB (screened by interferon-γ release assay and receiving anti-TB medication), no cases of active TB were reported. Moreover, an in vitro study examined the effect of the anti-tumor necrosis factor-α (TNFα) antibody adalimumab and secukinumab on dormant M. tuberculosis H37Rv in a novel human three-dimensional microgranuloma model. Auramine-O, Nile red staining and rifampicin resistance of M. tuberculosis were measured. In vitro, anti-TNFα treatment showed increased staining for Auramine-O, decreased Nile red staining and decreased rifampicin resistance, indicative of mycobacterial reactivation. In contrast, secukinumab treatment was comparable to control indicating a lack of effect on M. tuberculosis dormancy. To date, clinical and preclinical investigations with secukinumab found no evidence of increased M. tuberculosis infections.

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Yin and yang of interleukin-17 in host immunity to infection

Cited by 65 publications

References 177 publications

Interleukin-17 limits hypoxia-inducible factor 1α and development of hypoxic granulomas during tuberculosis

Interleukin-17 limits hypoxia-inducible factor 1α and development of hypoxic granulomas during tuberculosis

Immune predictors of mortality following RNA virus infection

Inhibition of IL‐17A by secukinumab shows no evidence of increased Mycobacterium tuberculosis infections

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