PMID- 16105040
OWN - NLM
STAT- MEDLINE
DCOM- 20060111
LR  - 20071114
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 68
IP  - 3
DP  - 2005 Sep
TI  - Antigen presentation by dendritic cells in renal lymph nodes is linked to 
      systemic and local injury to the kidney.
PG  - 1096-108
AB  - BACKGROUND: Dendritic cells (DCs) uniquely serve as conduits between innate and 
      cognate arms of the immune system. The normal kidney contains an extensive 
      population of interstitial DCs but their role in the pathogenesis of acute renal 
      injury is not known. METHODS: Renal DCs were studied by flow cytometric analysis 
      of collagenase-digested mouse kidneys, by immunohistochemistry, and by 
      immunofluorescence microscopy. In vivo ingestion by DCs of intravenously 
      administered fluorescein isothiocyanate (FITC)-dextran particles was examined. A 
      model antigen system (presentation of ovalbumin-derived peptide to TCR transgenic 
      CD4+ T-cells) was employed to examine the influence of systemic 
      (lipopolysacchride injection) and localized (unilateral renal artery clipping) 
      renal injury on DC-mediated T-cell activation in the renal lymph nodes (RLNs). 
      RESULTS: Renal DCs were shown to constitute the predominant source of T-cell 
      stimulatory capacity within the kidney, and to avidly ingest both filtered and 
      non-filtered particles. Lipopolysaccharide resulted in disappearance of DCs from 
      the renal interstitium within 48 hours. This was accompanied by increased renal 
      lymph node DCs, some of which contained intracellular Tamm-Horsfall Protein, 
      indicating abnormal trafficking of kidney-specific antigens following renal 
      injury. Lipopolysaccharide enhanced DC-mediated proliferation of 
      ovalbumin-specific CD4(+ve) T-cells within the draining RLN. Unilateral renal 
      ischemia augmented the capacity for DC-mediated T-cell activation in the lymph 
      nodes draining both the ischemic and nonischemic kidney. CONCLUSION: Renal DCs 
      respond to systemic or localized acute renal injury by increasing the traffic of 
      protein antigens from kidney to RLN, resulting in a concomitant increased 
      potential for localized activation of antigen-specific CD4(+ve) T-cells.
FAU - Dong, Xiangyang
AU  - Dong X
AD  - Division of Nephrology and Hypertension, Department of Medicine, Mayo Clinic 
      College of Medicine, Rochester, Minnesota 55905, USA.
FAU - Swaminathan, Sundararaman
AU  - Swaminathan S
FAU - Bachman, Lori A
AU  - Bachman LA
FAU - Croatt, Anthony J
AU  - Croatt AJ
FAU - Nath, Karl A
AU  - Nath KA
FAU - Griffin, Matthew D
AU  - Griffin MD
LA  - eng
GR  - D47060/PHS HHS/United States
GR  - DK68545/DK/NIDDK NIH HHS/United States
GR  - T32DK07013/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
SB  - IM
MH  - Animals
MH  - Antigen Presentation/*immunology
MH  - Antigen-Presenting Cells/immunology
MH  - CD4-Positive T-Lymphocytes/immunology
MH  - Cell Movement/immunology
MH  - Cells, Cultured
MH  - Dendritic Cells/*immunology
MH  - Ischemia/immunology/pathology
MH  - Kidney/*immunology
MH  - Kidney Diseases/*immunology/pathology
MH  - Lymph Nodes/cytology/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Phagocytes/immunology
EDAT- 2005/08/18 09:00
MHDA- 2006/01/13 09:00
CRDT- 2005/08/18 09:00
PHST- 2005/08/18 09:00 [pubmed]
PHST- 2006/01/13 09:00 [medline]
PHST- 2005/08/18 09:00 [entrez]
AID - S0085-2538(15)50937-X [pii]
AID - 10.1111/j.1523-1755.2005.00502.x [doi]
PST - ppublish
SO  - Kidney Int. 2005 Sep;68(3):1096-108. doi: 10.1111/j.1523-1755.2005.00502.x.