PMID- 12543882
OWN - NLM
STAT- MEDLINE
DCOM- 20030805
LR  - 20231213
IS  - 0931-0509 (Print)
IS  - 0931-0509 (Linking)
VI  - 18
IP  - 2
DP  - 2003 Feb
TI  - Upregulation of MHC class II, interferon-alpha and interferon-gamma receptor 
      protein expression in HIV-associated nephropathy.
PG  - 285-92
AB  - BACKGROUND: Renal cellular HIV infection has been linked to the pathogenesis of 
      HIV-associated nephropathy (HIVAN), but mediators of its development are unknown. 
      HIV infection is associated with disordered cytokine metabolism, and chemokine 
      receptors are coreceptors for HIV immune cellular infection. Chemokines such as 
      interleukin (IL)-8, monocyte chemoattractant protein-1 (MCP-1) and RANTES, and 
      interferons (IFNs) have been implicated in the progression of nephropathy. Renal 
      major histocompatibility complex (MHC) protein expression is involved in antigen 
      presentation and modulating tissue cellular immune responses. Their relative 
      importance in HIVAN pathogenesis is unknown. METHODS: We measured levels of 
      chemokines, IFN-alpha, IFN-gamma receptor and non-polymorphic MHC Class II 
      protein by high performance capillary electrophoresis, and incubation with 
      antibodies for quantification by chemiluminesce in renal tissue of patients with 
      HIVAN, compared with tissue without HIV infection, in the presence and absence of 
      nephropathy. Renal biopsy tissue protein levels were correlated with the number 
      and type of infiltrating tissue immune cells. RESULTS: Mean renal interstitial 
      and glomerular MCP-1, RANTES and IL-8 tissue levels were higher in patients with 
      HIV infection compared with tissue without HIV infection, regardless of the 
      presence of renal disease. In contrast, mean renal interstitial and glomerular 
      non-polymorphic MHC Class II, IFN-alpha and IFN-gamma receptor protein were 
      higher in patients with HIVAN compared with all other groups. Tissue MHC Class II 
      and IFN-gamma receptor protein levels did not correlate with immune cellular 
      infiltration in patients with HIV infection and renal disease. CONCLUSIONS: The 
      data suggest an upregulated renal immune microenvironment, capable of antigen 
      presentation, exists in HIVAN. MHC Class II proteins and IFNs, and the capacity 
      to present antigen may be crucial in HIVAN pathogenesis.
FAU - Kimmel, Paul L
AU  - Kimmel PL
AD  - Department of Medicine, Division of Renal Diseases and Hypertension, George 
      Washington University Medical Center, 2150 Pennsylvania Avenue NW, Washington, DC 
      20037, USA. pkimmel@mfa.gwu.edu
FAU - Cohen, David J
AU  - Cohen DJ
FAU - Abraham, A Andrew
AU  - Abraham AA
FAU - Bodi, Istvan
AU  - Bodi I
FAU - Schwartz, Arnold M
AU  - Schwartz AM
FAU - Phillips, Terry M
AU  - Phillips TM
LA  - eng
GR  - 1R01 DK 40811/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Nephrol Dial Transplant
JT  - Nephrology, dialysis, transplantation : official publication of the European 
      Dialysis and Transplant Association - European Renal Association
JID - 8706402
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Interferon-alpha)
RN  - 0 (Interleukin-8)
RN  - 0 (Receptors, Interferon)
SB  - IM
MH  - AIDS-Associated Nephropathy/*metabolism
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL5/metabolism
MH  - Glomerulosclerosis, Focal Segmental/metabolism
MH  - Histocompatibility Antigens Class II/*metabolism
MH  - Humans
MH  - Interferon-alpha/*metabolism
MH  - Interleukin-8/metabolism
MH  - Kidney/metabolism
MH  - Receptors, Interferon/*metabolism
MH  - Tissue Distribution
MH  - Up-Regulation
MH  - Interferon gamma Receptor
EDAT- 2003/01/25 04:00
MHDA- 2003/08/06 05:00
CRDT- 2003/01/25 04:00
PHST- 2003/01/25 04:00 [pubmed]
PHST- 2003/08/06 05:00 [medline]
PHST- 2003/01/25 04:00 [entrez]
AID - 10.1093/ndt/18.2.285 [doi]
PST - ppublish
SO  - Nephrol Dial Transplant. 2003 Feb;18(2):285-92. doi: 10.1093/ndt/18.2.285.