**4. Conclusions**

Innate immunity is the rapid host response and occurs within hours of microbial infections. Although a major role for innate immunity is to help dampen microbe replication until the adaptive immune response is adequately developed for final microbial elimination, another major role for innate immunity is to control and direct the developing adaptive immune response. There is substantial cross-talk between innate lymphocyte effectors during myocarditis. Both NKT and a population of γδ cells recognize CD1d, a non-classical MHC class I-like molecule. However, evidence implies that while NKT cells are protective in myocarditis, γδ cells are pro-inflammatory and pathogenic. Interesting similarities have been found in the role of NKT and γδ cells in two different myocarditis mouse models: CVB3 and Trypanosoma cruzi induced myocarditis. The fact that similar immune processes of pathogenicity and protection appear to function in these two models provides circumstantial evidence that these innate effectors may have identical roles in other forms of myocarditis and also in clinical disease. To date, little evidence actually exists for innate effectors in clinical disease. However, the strong association between microbial infections and myocarditis in humans means that innate immunity should be important.
