Target type: biologicalprocess
Any process that activates or increases the frequency, rate or extent of an antifungal innate immune response. [GO_REF:0000058, GOC:dph, GOC:TermGenie, PMID:22470487]
Positive regulation of antifungal innate immune response is a complex and essential biological process that involves a coordinated series of cellular and molecular events designed to detect and eliminate fungal pathogens. It is a critical component of host defense against fungal infections, which can range from superficial skin infections to life-threatening systemic diseases. This process is initiated upon recognition of fungal-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs) expressed on various immune cells, such as macrophages, neutrophils, and dendritic cells. These PRRs, including Toll-like receptors (TLRs), C-type lectin receptors (CLRs), and others, recognize specific fungal components like chitin, β-glucan, and mannan. Upon recognition, PRRs trigger downstream signaling pathways that lead to the activation of transcription factors, such as NF-κB and MAP kinases. These transcription factors induce the expression of a wide array of effector molecules, including cytokines, chemokines, and antimicrobial peptides. Cytokines, such as TNF-α, IL-1β, and IL-6, act as signaling molecules that recruit and activate other immune cells to the site of infection, further amplifying the immune response. Chemokines, like CCL2 and CXCL8, attract neutrophils and macrophages, which are essential for phagocytosis and killing of fungal cells. Antimicrobial peptides, including defensins and cathelicidins, directly kill fungal cells through disruption of their cell membrane. In addition to these immediate effector mechanisms, the activation of PRRs also leads to the production of reactive oxygen species (ROS) and nitric oxide (NO) by immune cells. These molecules have potent antifungal activity and contribute to the clearance of fungal pathogens. Furthermore, the process of positive regulation of antifungal innate immune response involves the activation of adaptive immune responses. Dendritic cells, which are professional antigen-presenting cells, engulf fungal antigens and present them to T lymphocytes. This interaction stimulates the differentiation of T helper cells (Th) into Th1 and Th17 cells, which produce cytokines like IFN-γ and IL-17, respectively. These cytokines further enhance the antifungal activity of macrophages and neutrophils, leading to a more robust and sustained immune response. The tight regulation of antifungal innate immune response is crucial for maintaining immune homeostasis and preventing excessive inflammation. This regulation involves various mechanisms, including the expression of inhibitory receptors, the production of anti-inflammatory cytokines, and the induction of tolerance mechanisms. Overall, positive regulation of antifungal innate immune response involves a complex network of interactions between immune cells, signaling pathways, and effector molecules. It is a vital process that protects the host from fungal infections, ensuring the successful elimination of these pathogens and the maintenance of host health.'
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Protein | Definition | Taxonomy |
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Phospholipase A2 group V | A phospholipase A2 group V that is encoded in the genome of human. [PRO:DNx, UniProtKB:P39877] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
3-octylthio-1,1,1-trifluoro-2-propanone | 3-octylthio-1,1,1-trifluoro-2-propanone: a pesticide synergist; inhibits juvenile hormone esterase | ||
varespladib | aromatic ether; benzenes; dicarboxylic acid monoamide; indoles; monocarboxylic acid; primary carboxamide | anti-inflammatory drug; antidote; EC 3.1.1.4 (phospholipase A2) inhibitor | |
ym 26734 | YM 26734: inhibits group II phospholipase A2; structure given in first source | ||
indoxam | indoxam: structure in first source |