PMID- 22219223
OWN - NLM
STAT- MEDLINE
DCOM- 20120525
LR  - 20220316
IS  - 1528-0020 (Electronic)
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 119
IP  - 13
DP  - 2012 Mar 29
TI  - Selective expansion of polyfunctional pathogen-specific CD4(+) T cells in 
      HIV-1-infected patients with immune reconstitution inflammatory syndrome.
PG  - 3105-12
LID - 10.1182/blood-2011-09-380840 [doi]
AB  - Since the introduction of highly active antiretroviral therapies (ART), the 
      prognosis for HIV-1 patients has improved immensely. However, approximately 25% 
      of patients can experience a variety of inflammatory symptoms that are 
      collectively known as immune reconstitution inflammatory syndrome (IRIS). 
      Studying the etiology and immunopathology of IRIS has been hampered by the fact 
      that the symptoms and associated opportunistic infections are highly varied. We 
      hypothesized that there is a common mechanism underlying IRIS pathogenesis and 
      investigated a patient group with IRIS related to different pathogens. Functional 
      and phenotypic characterization of PBMC samples was performed by polychromatic 
      flow cytometry after in vitro stimulation with relevant antigenic preparations. 
      In most patients, IRIS events were characterized by the robust increase of 
      preexisting polyfunctional, highly differentiated effector CD4(+) T-cell 
      responses that specifically targeted the antigens of the underlying co-infection. 
      T-cell responses to HIV-1 or other underlying infections were not affected and 
      did not differ between IRIS and non-IRIS patients. These data suggest that 
      patients with IRIS do not have a generalized T-cell dysfunction; instead, IRIS 
      represents a dysregulated CD4(+) T-cell response against residual opportunistic 
      infection antigen. These studies were registered at www.clinical-trials.gov as 
      NCT00557570 and NCT00286767.
FAU - Mahnke, Yolanda D
AU  - Mahnke YD
AD  - ImmunoTechnology Section, Vaccine Research Center, National Institute of Allergy 
      and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
FAU - Greenwald, Jamieson H
AU  - Greenwald JH
FAU - DerSimonian, Rebecca
AU  - DerSimonian R
FAU - Roby, Gregg
AU  - Roby G
FAU - Antonelli, Lis R V
AU  - Antonelli LR
FAU - Sher, Alan
AU  - Sher A
FAU - Roederer, Mario
AU  - Roederer M
FAU - Sereti, Irini
AU  - Sereti I
LA  - eng
SI  - ClinicalTrials.gov/NCT00286767
SI  - ClinicalTrials.gov/NCT00557570
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20120104
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
SB  - IM
CIN - Blood. 2012 Mar 29;119(13):2971-2. PMID: 22461468
MH  - AIDS-Related Opportunistic Infections/blood/etiology/immunology
MH  - Adult
MH  - CD4 Lymphocyte Count
MH  - CD4-Positive T-Lymphocytes/*immunology/pathology
MH  - CD8-Positive T-Lymphocytes/immunology/pathology
MH  - *Cell Proliferation
MH  - Female
MH  - HIV Infections/blood/complications/*immunology/virology
MH  - HIV-1/*immunology/pathogenicity/physiology
MH  - Humans
MH  - Immune Reconstitution Inflammatory Syndrome/blood/etiology/*immunology/virology
MH  - Longitudinal Studies
MH  - Male
MH  - T-Cell Antigen Receptor Specificity/immunology
MH  - Viral Load
PMC - PMC3321870
EDAT- 2012/01/06 06:00
MHDA- 2012/05/26 06:00
PMCR- 2013/03/29
CRDT- 2012/01/06 06:00
PHST- 2012/01/06 06:00 [entrez]
PHST- 2012/01/06 06:00 [pubmed]
PHST- 2012/05/26 06:00 [medline]
PHST- 2013/03/29 00:00 [pmc-release]
AID - S0006-4971(20)49179-7 [pii]
AID - 2011/380840 [pii]
AID - 10.1182/blood-2011-09-380840 [doi]
PST - ppublish
SO  - Blood. 2012 Mar 29;119(13):3105-12. doi: 10.1182/blood-2011-09-380840. Epub 2012 
      Jan 4.