Anti-fungal immune response mechanism is

Fungi widespread and we live in an environment, our health they also have an important impact. Our lungs are constantly exposed to the air, and thus come into contact with a large number of Aspergillus and Fusarium spores, and thus lead to infection; mucosal system we also often have symbiotic fungi exist, including the like Candida and mold. Aspergillus and Fusarium infections are the main cause of blindness corneal ulcer disease. Overall, the annual population suffering from a fungal infection accounted for 25% of the world's population, some serious diseases (candidiasis, pneumocystosis, cryptococcosis) disease each year with more than 2 million, more than 50% mortality rate. Therefore, the severity of malaria and fungal infections as much as Mycobacterium tuberculosis infection. Depth understanding of our immune systems, and the characteristics of the interaction of microorganisms with the outside world can help to take effective measures to prevent fungal infections. David M. Underhill professors from Los Angeles Cedars-Sinai Medical Center and the University of California, Irvine immunization of Eric Pearlman on "immunity" magazine published a review article, fungal and immune system interactions in detail Discussion.
With the long-term evolution, the human immune system against infection of the external environment has developed a variety of different immunization strategies. Through the crowd to do the analysis of genetics, combined with their resistance to fungal infection tolerance to find relevant genes. First, phagocytosis in cellular immune defects associated with increased fungal infections. For example: Defect NAPDH protein (a protein capable of generating reactive oxygen component), or a defect mutation neutrophils, can lead to fungal infections. This shows that the role of neutrophils in the anti-fungal infection. Humoral contribution is relatively small, but studies have shown antibodies for anti-fungal infection also has a significant role.
HIV patients often cause some fungal infections, such as oral candidiasis or pneumocystosis. This shows that T cells to anti-fungal infection also has an important role. A recent study found: Mycobacterium tuberculosis infection in susceptible patients in vivo RORC gene mutations, mutations in this gene cause the patient lacks functional RORgamma or RORgamma t, and cause the lymph nodes to induce the missing cells. RORgamma t cells to produce IL-17 is important, so that these patients can not produce IL-17.
A very long time to, lectins (lectin) is considered a key component of fungal infection process. 1060, Miller et al., First found to reduce the expression of mannose binding lectin serum could destroy yeast lysis active ingredient. Since then, a number of studies indicate Dectin1 (a class of C-type lectin receptor) for mucosal candidiasis infection plays an important role. The researchers found that patients with a CARD9 (connected downstream of the C type lectin molecule) defects can cause more serious Candida infections. CARD9 defect can also lead to reduction of Th17 cells and the corresponding cytokine and chemokine production.
Some studies have found that Toll like receptor also plays an important role in fungal infections, including TLR-1, TLR4, TLR6 like.
Inflammatory cytokines IL-1beta release depends on the activation of intracellular inflammation of small bodies as well as IL-1beta precursors cutting. The study found that the mutation NLRP3 (inflammation of the small body) gene can lead to female genital vestibulitis and vulvar candidiasis.
In short, by genetic mutations mass analysis can be found with the active immune signaling molecule has an important impact on the fungal infection.
After that, the author of C-type lectin receptors in the anti-fungal immune responses as well as the main mechanism of antifungal cytokine critical to do a detailed discussion will not go