PMID- 30555775
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220330
IS  - 2196-5471 (Print)
IS  - 2196-5471 (Electronic)
IS  - 2196-5471 (Linking)
VI  - 5
IP  - 3
DP  - 2018 Sep
TI  - Understanding mechanisms underlying the pathology of immune reconstitution 
      inflammatory syndrome (IRIS) by using animal models.
PG  - 201-209
LID - 10.1007/s40588-018-0099-5 [doi]
AB  - PURPOSE OF REVIEW: Despite the increasing number of clinical reports on immune 
      reconstitution inflammatory syndrome (IRIS), mechanistic understanding of IRIS is 
      still largely limited. The main focus of this review is to summarize animal 
      studies, which were performed to better understand the cellular and molecular 
      mechanisms underlying the pathology of IRIS. RECENT FINDINGS: Three IRIS animal 
      models have been reported. They are Mycobacterial IRIS (M-IRIS), cryptococcal 
      IRIS (C-IRIS) and Pneumocystis-IRIS. M-IRIS animal model suggested that, rather 
      than lymphopenia itself, the failure to clear the pathogen by T cells results in 
      excessive priming of the innate immune system. If this happens before T cell 
      reconstitution, hosts likely suffer IRIS upon T cell reconstitution. 
      Interestingly, T cells specific to self-antigens, not only pathogen-specific, 
      could drive IRIS as well. SUMMARY: The mechanism to develop IRIS is quite 
      complicated, including multiple layers of host immune responses; the innate 
      immune system that detects pathogens and prime host immunity, and the adaptive 
      immune system that is reconstituted but hyper-activated particularly through 
      CD4(+) T cells. Animal models of IRIS, although there are still small numbers of 
      studies available, have already provided significant insights on the mechanistic 
      understanding of IRIS.
FAU - Aggarwal, Nupur
AU  - Aggarwal N
AD  - Duke University School of Medicine, Department of Immunology, Durham, NC, USA.
FAU - Barclay, William
AU  - Barclay W
AD  - Duke University School of Medicine, Department of Immunology, Durham, NC, USA.
FAU - Shinohara, Mari L
AU  - Shinohara ML
AD  - Duke University School of Medicine, Department of Immunology, Durham, NC, USA.
AD  - Duke University School of Medicine, Department of Molecular Genetics and 
      Microbiology, Durham, NC, USA.
LA  - eng
GR  - R01 AI088100/AI/NIAID NIH HHS/United States
GR  - R21 AI135999/AI/NIAID NIH HHS/United States
GR  - T32 AI052077/AI/NIAID NIH HHS/United States
PT  - Journal Article
DEP - 20180622
PL  - Switzerland
TA  - Curr Clin Microbiol Rep
JT  - Current clinical microbiology reports
JID - 101642669
PMC - PMC6291227
MID - NIHMS977369
OTO - NOTNLM
OT  - Cryptococcus neoformans
OT  - IRIS
OT  - Immune reconstitution
OT  - Mycobacterium avium
OT  - Opportunistic infection
OT  - Pneumocystis
EDAT- 2018/12/18 06:00
MHDA- 2018/12/18 06:01
PMCR- 2019/09/01
CRDT- 2018/12/18 06:00
PHST- 2018/12/18 06:00 [entrez]
PHST- 2018/12/18 06:00 [pubmed]
PHST- 2018/12/18 06:01 [medline]
PHST- 2019/09/01 00:00 [pmc-release]
AID - 10.1007/s40588-018-0099-5 [doi]
PST - ppublish
SO  - Curr Clin Microbiol Rep. 2018 Sep;5(3):201-209. doi: 10.1007/s40588-018-0099-5. 
      Epub 2018 Jun 22.