Mast cells (MCs), which are well known for their effector functions in T H 2-skewed allergic and also autoimmune inflammation, have become increasingly acknowledged for their role in protection of health. It is now clear that they are also key modulators of immune responses at interface organs, such as the skin or gut. MCs can prime tissues for adequate inflammatory responses and cooperate with dendritic cells in T-cell activation. They also regulate harmful immune responses in trauma and help to successfully orchestrate pregnancy. This review focuses on the beneficial effects of MCs on tissue homeostasis and elimination of toxins or venoms. MCs can enhance pathogen clearance in many bacterial, viral, and parasitic infections, such as through Toll-like receptor 2-triggered degranulation, secretion of antimicrobial cathelicidins, neutrophil recruitment, or provision of extracellular DNA traps. The role of MCs in tumors is more ambiguous; however, encouraging new findings show they can change the tumor microenvironment toward antitumor immunity when adequately triggered. Uterine tissue remodeling by a-chymase (mast cell protease [MCP] 5) is crucial for successful embryo implantation. MCP-4 and the tryptase MCP-6 emerge to be protective in central nervous system trauma by reducing inflammatory damage and excessive scar formation, thereby protecting axon growth. Last but not least, proteases, such as carboxypeptidase A, released by FcεRIactivated MCs detoxify an increasing number of venoms and endogenous toxins. A better understanding of the plasticity of MCs will help improve these advantageous effects and hint at ways to cut down detrimental MC actions.
Abecasis GR, Cherny SS, Cookson WO et al. (2002) Merlin-rapid analysis of dense genetic maps using sparse gene flow trees. Nat Genet 30:97-101 Bapat B, Xia L, Madlensky L et al. (1996) The genetic basis of Muir-Torre syndrome includes the hMLH1 locus. Am J Hum Genet 59:736-9 Chakrabarty KH, Perks AG (1996) Ferguson-Smith syndrome: the importance of long term follow-up. Br J Plast Surg 49:497-8 Cribier B, Asch P, Grosshans E (1999) Differentiating squamous cell carcinoma from keratoacanthoma using histopathological criteria. Is it possible? A study of 296 cases. Dermatology 199:208-12 Feldman RJ, Maize JC (2007) Multiple keratoacanthomas in a young woman: report of a case emphasizing medical management and a review of the spectrum of multiple keratoacanthomas. Int J Dermatol 46:77-9 Giglia-Mari G, Sarasin A (2003) TP53 mutations in human skin cancers. Hum Mutat 21: 217-28 Goudie DR, D'Alessandro M, Merriman B et al. (2011) Multiple self-healing squamous epithelioma is caused by a disease-specific spectrum of mutations in TGFBR1. Nat Genet 43:365-9 Grzybowski (1950) A case of peculiar generalised epithelial tumors of the skin. Br J Dermatol 63:310-3 Kruse R, Rutten A, Lamberti C et al. (1998) Muir-Torre phenotype has a frequency of DNA mismatch-repair-gene mutations similar to that in hereditary nonpolyposis colorectal cancer families defined by the Amsterdam criteria. Am J Hum Genet 63:63-70 Muir E, Bell A, Barlow K (1967) Multiple primary carcinomata of the colon, duodenum, and larynx associated with keratoacanthomata of the face.
E, et al. Bypassing hybridoma technology: HLA-C reactive human single-chain antibody fragments (scFv) derived from a synthetic phage display library (HuCAL) and their potential to discriminate HLA class I specificities. Tissue Antigens 2000;56:1e9. Meister M, Tounsi A, Gaffal E, Bald T, Papatriantafyllou M, Ludwig J, et al. Self-antigen presentation by keratinocytes in the inflamed adult skin modulates T-cell autoreactivity.
Proinflammatory IL‐17 plays an important role in various diseases and defence against extracellular microorganisms. Healing of leishmaniasis is promoted by Th1/Tc1 cells, whereas Th2/Treg are associated with worsened disease outcome. In addition, high expression of IL‐17A in Leishmania‐susceptible BALB/c and artificial overexpression of IL‐17A in T cells in resistant C57BL/6 mice worsened disease outcome. Since C57BL/6 mice lacking only IL‐17A exhibited no phenotype, and IL‐17A and IL‐17F share similar receptors, but differentially regulate chemokine secretion, we studied mice lacking both IL‐17A and IL‐17F (IL‐17A/F−/−) in infections with Leishmania major. Interestingly, lesion volumes and parasite burdens were comparable to controls, IL‐17A/F−/− mice developed a Th1/Tc1 phenotype, and exhibited normal lesion resolution. Thus, in C57BL/6 mice, secretion of IL‐17A and IL‐17F does not influence disease progression. It appears that—depending on the genetic background—cytokines of the IL‐17 family might be responsible for disease progression primarily in susceptible mice.
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