We are analyzing https://link.springer.com/article/10.1186/ar3893.

Title:
Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy | Arthritis Research & Therapy
Description:
IL-17 and related cytokines are direct and indirect targets of selective immunosuppressive agents for the treatment of autoimmune diseases and other diseases of pathologic inflammation. Insights into the potential adverse effects of IL-17 blockade can be drawn from the experience of patients with deficiencies in the IL-17 pathway. A unifying theme of susceptibility to mucocutaneous candidiasis is seen in both mice and humans with a variety of genetic defects that converge on this pathway. Mucocutaneous candidiasis is a superficial infection of mucosal, nail or skin surfaces usually caused by the fungal pathogen Candida albicans. The morbidity of the disease includes significant pain, weight loss and secondary complications, including carcinoma and aneurysms. This review describes the known human diseases associated with chronic mucocutaneous candidiasis (CMC) as well as the known and proposed connections to IL-17 signaling. The human diseases include defects in IL-17 signaling due to autoantibodies (AIRE deficiency), receptor mutations (IL-17 receptor mutations) or mutations in the cytokine genes (IL17F and IL17A). Hyper-IgE syndrome is characterized by elevated serum IgE, dermatitis and recurrent infections, including CMC due to impaired generation of IL-17-producing Th17 cells. Mutations in STAT1, IL12B and IL12RB1 result in CMC secondary to decreased IL-17 production through different mechanisms. Dectin-1 defects and CARD9 defects result in susceptibility to C. albicans because of impaired host recognition of the pathogen and subsequent impaired generation of IL-17-producing T cells. Thus, recent discoveries of genetic predisposition to CMC have driven the recognition of the role of IL-17 in protection from mucosal fungal infection and should guide counseling and management of patients treated with pharmacologic IL-17 blockade.
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Keywords {🔍}

pubmed, article, google, scholar, cas, candidiasis, patients, cmc, cells, mucocutaneous, central, susceptibility, mutations, disease, immunity, stat, infections, chronic, receptor, pathway, deficiency, med, ila, fungal, albicans, cytokines, autoimmune, defects, candida, immunol, signaling, ilf, mutation, arthritis, human, oral, diseases, mice, mucosal, dectin, family, cell, syndrome, including, card, clinical, infection, immune, normal, ilra,

Topics {✒️}

c-type lectin receptors autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy mitogen-activated protein kinase lower fungal-sensing capacity regulating anti-fungal immunity anti interleukin-17-receptor antibody il12rb1 gene products tumor necrosis factor innate anti-fungal immunity growth-regulated oncogene-α ifn-gamma-mediated immunity innate lymphoid cells t-cell receptor signaling oral squamous-cell carcinoma symptomatic cytomegalo-virus infection chronic mucocutaneous candidiasis gram-negative bacterial pneumonia nf-κb activity leads dectin-1-deficient cohort suggests impaired t-cell activation mutant il-17f identified anti-cytokine antibodies disrupt il12rb1 gene encodes genome-wide approach based anti-cytokine autoantibodies produced author information authors mucocutaneous fungal infections randomised placebo-controlled trials termed mucocutaneous candidiasis conti hr unusual auto-immune diseases bacterial sino-pulmonary infections common anti-cytokine autoantibodies anti-fungal agents spleen tyrosine kinase shared il-12/23p40 subunit privacy choices/manage cookies chronic plaque psoriasis long-term safety experience neck radiation therapy squamous cell carcinoma population-wide search su hc stat-1-dependent genes mucosal fungal infection innate il-17-producing cells t-cell activation multiple genes related caspase recruitment domain curr opin microbiol

Questions {❓}

Puel A, Picard C, Cypowyj S, Lilic D, Abel L, Casanova JL: Inborn errors of mucocutaneous immunity to Candida albicans in humans: a role for IL-17 cytokines?

Schema {🗺️}

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         headline:Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy
         description:IL-17 and related cytokines are direct and indirect targets of selective immunosuppressive agents for the treatment of autoimmune diseases and other diseases of pathologic inflammation. Insights into the potential adverse effects of IL-17 blockade can be drawn from the experience of patients with deficiencies in the IL-17 pathway. A unifying theme of susceptibility to mucocutaneous candidiasis is seen in both mice and humans with a variety of genetic defects that converge on this pathway. Mucocutaneous candidiasis is a superficial infection of mucosal, nail or skin surfaces usually caused by the fungal pathogen Candida albicans. The morbidity of the disease includes significant pain, weight loss and secondary complications, including carcinoma and aneurysms. This review describes the known human diseases associated with chronic mucocutaneous candidiasis (CMC) as well as the known and proposed connections to IL-17 signaling. The human diseases include defects in IL-17 signaling due to autoantibodies (AIRE deficiency), receptor mutations (IL-17 receptor mutations) or mutations in the cytokine genes (IL17F and IL17A). Hyper-IgE syndrome is characterized by elevated serum IgE, dermatitis and recurrent infections, including CMC due to impaired generation of IL-17-producing Th17 cells. Mutations in STAT1, IL12B and IL12RB1 result in CMC secondary to decreased IL-17 production through different mechanisms. Dectin-1 defects and CARD9 defects result in susceptibility to C. albicans because of impaired host recognition of the pathogen and subsequent impaired generation of IL-17-producing T cells. Thus, recent discoveries of genetic predisposition to CMC have driven the recognition of the role of IL-17 in protection from mucosal fungal infection and should guide counseling and management of patients treated with pharmacologic IL-17 blockade.
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      headline:Mucocutaneous candidiasis: the IL-17 pathway and implications for targeted immunotherapy
      description:IL-17 and related cytokines are direct and indirect targets of selective immunosuppressive agents for the treatment of autoimmune diseases and other diseases of pathologic inflammation. Insights into the potential adverse effects of IL-17 blockade can be drawn from the experience of patients with deficiencies in the IL-17 pathway. A unifying theme of susceptibility to mucocutaneous candidiasis is seen in both mice and humans with a variety of genetic defects that converge on this pathway. Mucocutaneous candidiasis is a superficial infection of mucosal, nail or skin surfaces usually caused by the fungal pathogen Candida albicans. The morbidity of the disease includes significant pain, weight loss and secondary complications, including carcinoma and aneurysms. This review describes the known human diseases associated with chronic mucocutaneous candidiasis (CMC) as well as the known and proposed connections to IL-17 signaling. The human diseases include defects in IL-17 signaling due to autoantibodies (AIRE deficiency), receptor mutations (IL-17 receptor mutations) or mutations in the cytokine genes (IL17F and IL17A). Hyper-IgE syndrome is characterized by elevated serum IgE, dermatitis and recurrent infections, including CMC due to impaired generation of IL-17-producing Th17 cells. Mutations in STAT1, IL12B and IL12RB1 result in CMC secondary to decreased IL-17 production through different mechanisms. Dectin-1 defects and CARD9 defects result in susceptibility to C. albicans because of impaired host recognition of the pathogen and subsequent impaired generation of IL-17-producing T cells. Thus, recent discoveries of genetic predisposition to CMC have driven the recognition of the role of IL-17 in protection from mucosal fungal infection and should guide counseling and management of patients treated with pharmacologic IL-17 blockade.
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         Chronic Mucocutaneous Candidiasis
         Lymphoid Tissue Inducer Cell
         IL12RB1 Gene
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         Orthopedics
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