Adaptive immune responses to<i>Candida albicans</i>infection

Richardson, Jonathan P.; Moyes, David L.

doi:10.1080/21505594.2015.1004977

Cited by 157 publications

(152 citation statements)

References 122 publications

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“…These cytokines are produced as inactive precursors that undergo caspase‐mediated cleavage to yield biologically active molecules. Although inflammasome activity is associated with innate immunity, the production of functionally mature IL‐1 β and IL‐18 influences the outcome of the adaptive immunity, so, affecting Th17 and Th1 responses, respectively . As expected, the IL‐1 β release in all the KO groups (NLRP3 −/− , ASC −/− and caspase‐1 −/− ) was markedly diminished, suggesting the inflammasome‐driven release of this cytokine during the S. schenckii infection is exclusively dependent on the NLRP3 inflammasome.…”

Section: Discussionsupporting

confidence: 66%

The NLRP3 inflammasome contributes to host protection during Sporothrix schenckii infection

et al. 2017

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Sporotrichosis is a mycosis caused by fungi from the Sporothrix schenckii species complex, whose prototypical member is Sporothrix schenckii sensu stricto. Pattern recognition receptors (PRRs) recognize and respond to pathogen-associated molecular patterns (PAMPs) and shape the following adaptive immune response. A family of PRRs most frequently associated with fungal recognition is the nucleotide-binding oligomerization domain-like receptor (NLR). After PAMP recognition, NLR family pyrin domain-containing 3 (NLRP3) binds to apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and caspase-1 to form the NLRP3 inflammasome. When activated, this complex promotes the maturation of the pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18 and cell death through pyroptosis. In this study, we aimed to evaluate the importance of the NLRP3 inflammasome in the outcome of S. schenckii infection using the following three different knockout (KO) mice: NLRP3 , ASC and caspase-1 . All KO mice were more susceptible to infection than the wild-type, suggesting that NLRP3-triggered responses contribute to host protection during S. schenckii infection. Furthermore, the NLRP3 inflammasome appeared to be critical for the ex vivo release of IL-1β, IL-18 and IL-17 but not interferon-γ. Additionally, a role for the inflammasome in shaping the adaptive immune response was suggested by the lower frequencies of type 17 helper T (Th17) cells and Th1/Th17 but not Th1 cells in S. schenckii-infected KO mice. Overall, our results indicate that the NLRP3 inflammasome links the innate recognition of S. schenckii to the adaptive immune response, so contributing to protection against this infection.

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Section: Discussionsupporting

confidence: 66%

The NLRP3 inflammasome contributes to host protection during Sporothrix schenckii infection

et al. 2017

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“…Although antibody responses to C. albicans infection are thought to have a relatively minor role in immune protection, they are significantly less effective than cellular responses (Richardson and Moyes, 2015), and the direct candidacidal activity of some antibodies elicited against C. albicans is of great interest, especially for the prevention and even treatment of Candida infections in immunocompromised patients (Cabezas et al, 2010). Although antibody responses to C. albicans infection are thought to have a relatively minor role in immune protection, they are significantly less effective than cellular responses (Richardson and Moyes, 2015), and the direct candidacidal activity of some antibodies elicited against C. albicans is of great interest, especially for the prevention and even treatment of Candida infections in immunocompromised patients (Cabezas et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

The evaluation of β-(1 → 3)-nonaglucoside as an anti-Candida albicansimmune response inducer

Paulovičová

Pilišiová

et al. 2016

Cellular Microbiology

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Synthetically prepared bovine serum albumin (BSA) conjugate of linear β-(1 → 3)-nonaglucoside ligand (G9) has been applied as a biological response immunomodulator in vivo and ex vivo. Active immunization of Balb/c mice revealed effective induction of specific humoral responses in comparison with Candida β-D-glucan and Candida whole cells. Induced post-vaccination serum exhibited a growth-inhibition effect on the multi-azole-resistant clinical strain Candida albicans CCY 29-3-164 in experimental mucocutaneous infection ex vivo. Evaluation of immune cell proliferation and the cytotoxic potential of the G9-ligand has revealed its bioavailability and an immunostimulative effect in vaccination-sensitized Balb/c mice splenocytes and RAW 264.7 macrophages.

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“…Defects in IL-17-mediated immunity due to germline mutations, including IL-17-related genes such as IL17F and IL17RA, loss-of-function mutations in STAT3, gain-of-function mutations in STAT1, mutations in AIRE, and patients with autoimmune polyendocrinopathy syndrome-1 have been implicated in difficulty in clearing certain types of bacterial and fungal infections (60)(61)(62). In particular, individuals with defects in IL-17-mediated immunity often have chronic or repeated mucocutaneous candidiasis, suggesting that an effective Th17 response is essential to controlling commensal C. albicans.…”

Section: Discussionmentioning

confidence: 99%