PMID- 27085555
OWN - NLM
STAT- MEDLINE
DCOM- 20170814
LR  - 20180114
IS  - 1532-8392 (Electronic)
IS  - 0046-8177 (Linking)
VI  - 54
DP  - 2016 Aug
TI  - Dendritic cells in renal biopsies of patients with acute tubulointerstitial 
      nephritis.
PG  - 113-20
LID - S0046-8177(16)30039-9 [pii]
LID - 10.1016/j.humpath.2016.03.020 [doi]
AB  - Dendritic cells (DCs) play a critical role in the regulation of the adaptive 
      immune response and can be separated into 2 major subsets: myeloid (mDC) and 
      plasmacytoid (pDC) DCs. Acute tubulointerstitial nephritis (ATIN) is a common 
      cause of injury to renal tubules and interstitium resulting from the interplay of 
      tubular cells and inflammatory cells and their products. However, the involvement 
      of DCs in ATIN is still unknown. In this study, the participation and 
      localization of myeloid (CD1c) and plasmacytoid (CD303) DC subsets in the 
      biopsies from patients with ATIN (n=20), lupus nephritis (n=17, positive 
      control), or minimal change disease (n=14, negative control) were investigated. 
      DCs were identified morphologically within the tubulointerstitium in the renal 
      biopsies by transmission electron microscopy interacting with surrounding tubules 
      and inflammatory cells. Direct immunofluorescence showed that both CD1c+DCs and 
      CD303+ DCs exist in all the renal biopsies. As compared with minimal change 
      disease, biopsies with ATIN had significantly increased CD1c+DCs (P<.001) and 
      CD303+ DCs (P<.001). The number of CD1c+DCs in ATIN was significantly higher than 
      that in lupus nephritis (P<.02), whereas the number of CD303+ DCs in ATIN was 
      slightly but not significantly higher than that in lupus nephritis (P=.2). DCs in 
      the biopsies with ATIN were restricted to the tubulointerstitium forming dense 
      networks, and most of them maintained immature state. All these findings suggest 
      that DC subsets may be differentially involved in the pathogenesis of ATIN. Their 
      potential role in intrarenal regulation of immune responses in ATIN is proposed.
CI  - Copyright (c) 2016 Elsevier Inc. All rights reserved.
FAU - Cheng, Mingyu
AU  - Cheng M
AD  - Department of Pathology and Translational Pathobiology, Louisiana State 
      University Health Sciences Center, Shreveport, LA 71103.
FAU - Gu, Xin
AU  - Gu X
AD  - Department of Pathology and Translational Pathobiology, Louisiana State 
      University Health Sciences Center, Shreveport, LA 71103.
FAU - Herrera, Guillermo A
AU  - Herrera GA
AD  - Department of Pathology and Translational Pathobiology, Louisiana State 
      University Health Sciences Center, Shreveport, LA 71103. Electronic address: 
      gherr1@lsuhsc.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160413
PL  - United States
TA  - Hum Pathol
JT  - Human pathology
JID - 9421547
RN  - 0 (Antigens, CD1)
RN  - 0 (Biomarkers)
RN  - 0 (CD1C protein, human)
RN  - 0 (CLEC4C protein, human)
RN  - 0 (Glycoproteins)
RN  - 0 (Lectins, C-Type)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Immunologic)
RN  - Acute Tubulointerstitial Nephritis
SB  - IM
MH  - Antigens, CD1/analysis
MH  - Biomarkers/analysis
MH  - Biopsy
MH  - Dendritic Cells/immunology/*ultrastructure
MH  - Fluorescent Antibody Technique
MH  - Glycoproteins/analysis
MH  - Humans
MH  - Kidney Tubules/immunology/*ultrastructure
MH  - Lectins, C-Type/analysis
MH  - Membrane Glycoproteins/analysis
MH  - Microscopy, Electron, Transmission
MH  - Nephritis, Interstitial/immunology/*pathology
MH  - Phenotype
MH  - Receptors, Immunologic/analysis
OTO - NOTNLM
OT  - Acute tubulointerstial nephritis
OT  - Dendritic cells
OT  - Immune modulation
OT  - Myeloid
OT  - Plasmacytoid
EDAT- 2016/04/18 06:00
MHDA- 2017/08/15 06:00
CRDT- 2016/04/18 06:00
PHST- 2016/01/12 00:00 [received]
PHST- 2016/03/24 00:00 [revised]
PHST- 2016/03/31 00:00 [accepted]
PHST- 2016/04/18 06:00 [entrez]
PHST- 2016/04/18 06:00 [pubmed]
PHST- 2017/08/15 06:00 [medline]
AID - S0046-8177(16)30039-9 [pii]
AID - 10.1016/j.humpath.2016.03.020 [doi]
PST - ppublish
SO  - Hum Pathol. 2016 Aug;54:113-20. doi: 10.1016/j.humpath.2016.03.020. Epub 2016 Apr 
      13.