[Mast cells in viral infections].
There are some premises suggesting that mast cells are involved in the mechanisms of anti-virus defense and in viral disease pathomechanisms. Mast cells are particularly numerous at the portals of infections and thus may have immediate and easy contact with the external environment and invading pathogens. These cells express receptors responsible for recognition of virus-derived PAMP molecules, mainly Toll-like receptors (TLR3, TLR7/8 and TLR9), but also RIG-I-like and NOD-like molecules. Furthermore, mast cells generate various mediators, cytokines and chemokines which modulate the intensity of inflammation and regulate the course of innate and adaptive anti-viral immunity. Indirect evidence for the role of mast cells in viral infections is also provided by clinical observations and results of animal studies. Currently, more and more data indicate that mast cells can be infected by some viruses (dengue virus, adenoviruses, hantaviruses, cytomegaloviruses, reoviruses, HIV-1 virus). It is also demonstrated that mast cells can release pre formed mediators as well as synthesize de novo eicosanoids in response to stimulation by viruses. Several data indicate that virus-stimulated mast cells secrete cytokines and chemokines, including interferons as well as chemokines with a key role in NK and Tc lymphocyte influx. Moreover, some information indicates that mast cell stimulation via TLR3, TLR7/8 and TLR9 can affect their adhesion to extracellular matrix proteins and chemotaxis, and influence expression of some membrane molecules. Critical analysis of current data leads to the conclusion that it is not yet possible to make definitive statements about the role of mast cells in innate and acquired defense mechanisms developing in the course of viral infection and/or pathomechanisms of viral diseases.
Zakład Immunologii Doświadczalnej, Uniwersytet Medyczny w Łodzi.
Piotr
P
Witczak
Ewa
E
Brzezińska-Błaszczyk
D000998:Antiviral Agents; D018925:Chemokines / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D003716:Dengue Virus / Q000378:metabolism; D015658:HIV Infections / Q000378:metabolism; D015497:HIV-1 / Q000378:metabolism; D006801:Humans; D058847:Inflammasomes / Q000276:immunology; D007372:Interferons / Q000096:biosynthesis; D008407:Mast Cells / Q000276:immunology*; D051193:Toll-Like Receptors / Q000096:biosynthesis / Q000276:immunology; D014777:Virus Diseases / Q000276:immunology*
D000998:Antiviral Agents; D018925:Chemokines; D016207:Cytokines; D058847:Inflammasomes; D051193:Toll-Like Receptors; D007372:Interferons