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               dissemination of virus, bacteria, parasite or fungus, or meningitis in which natural barriers are lost .
                                                                                                        [11]
               Autophagy activation in this situation may be due to adaptive immune signalling through pattern recognition
               or by secretive pro-inflammatory cytokines (for example tumor necrosis factor-α and interferon-γ) following
               infections . Autophagy can go in both ways, its activation may clear the micro-organism or the micro-
                        [12]
               organism may use autophagic activation for their benefit and survival . This immune mediated autophagic
                                                                          [12]
               process is highly regulated by a number of up and down regulating genes . This may be the reason why
                                                                               [13]
               some organisms provide different disease severity in different individuals or even in the same individual
               in the subsequent infection. There are many unresolved questions - Does the different organ system have
               customized autophagy operating system or have uniform operating system? How much autophagy activation
               is needed for clearance of pathogens and development of protective adaptive immunity? Is it possible to
               explore the survival autophagy response in adverse situation, the way saprophytic bacteria lives days to
               years? The resolution of these questions may pave the way for potential new treatment.



               DECLARATIONS
               Acknowledgments
               We thanks Mr. Shakti Kumar for secretarial help.


               Authors’ contributions
               Concept, literature search, manuscript preparation and review: Kalita J
               Concept, manuscript review: Misra UK
               Literature search, manuscript review: Kumar A


               Financial support and sponsorship
               None.


               Conflicts of interest
               There are no conflicts of interest.


               Patient consent
               Not applicable.


               Ethics approval
               Not applicable.


               Copyright
               © The Author(s) 2018.



               REFERENCES
               1.   Takeshige K, Baba M, Tsuboi S, Noda T, Ohsumi Y. Autophagy in yeast demonstrated with proteinase-deficient mutants and conditions
                   for its induction. J Cell Biol 1992;119:301-11.
               2.   He SY, Wang CD, Dong HY, Xia FC, Zhou H, Jiang XS, Pei CY, Ren H, Li HS, Li R, Xu HW. Immune-related GTPase M (IRGM1)
                   regulates neuronal autophagy in a mouse model of stroke. Autophagy 2012;8:1621-7.
               3.   Alam J, Scheper W. Targeting neuronal MAPK14/p38α activity to modulate autophagy in the Alzheimer disease brain. Autophagy
                   2016;12:2516-20.
               4.   Ahmed I, Liang YD, Schools S, Dawson VL, Dawson TM, Savitt JM. Development and characterization of a new Parkinson disease
                   model resulting from impaired autophagy. J Neurosci 2012;32:16503-9.
               5.   Pratt ZL, Sugden B. How human tumor viruses make use of autophagy. Cells 2012;1:617-30.
               6.   Katzenell S, Leib DA. Herpes simplex virus and interferon signaling induce novel autophagic clusters in sensory neurons. J Virol
                   2016;90:4706-19.
               7.   Yuk JM, Yoshimori T, Jo EK. Autophagy and bacterial infectious diseases. Exp Mol Med 2012;44:99-108.
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