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Expression of IFN‐γ induced CXCR3 agonist chemokines and compartmentalization of CXCR3 + cells in the periphery and lymph nodes of rhesus macaques during simian immunodeficiency virus infection and acquired immunodeficiency syndrome
Author(s) -
Sarkar Surojit,
Kalia Vandana,
MurpheyCorb Michael,
Montelaro Ronald C.,
Reinhart Todd A.
Publication year - 2003
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1034/j.1600-0684.2003.00031.x
Subject(s) - cxcl10 , cxcr3 , simian immunodeficiency virus , immunology , chemokine , biology , chemokine receptor , lymph , flow cytometry , cxcl9 , t cell , virology , virus , medicine , pathology , immune system
  Dysregulation of cytokines and chemokines during human immunodeficiency virus 1 (HIV‐1) and simian immunodeficiency virus (SIV) infection is thought to be critical in the progression of acquired immunodeficiency syndrome (AIDS). To evaluate the potential role of Th1‐agonist chemokines in disease progression during AIDS, we assessed CXCL9/MIG and CXCL10/IP‐10 expression simultaneously in the periphery and lymphoid tissues of SIV‐infected animals at a single‐cell level by flow cytometry. We optimized intracellular staining and analysis of CXCL9/MIG and CXCL10/IP‐10 production in human leukocyte antigen (HLA)‐DR + macaque cells by flow cytometry using cross‐reactive antibodies against human chemokines. We observed an upregulation of CXCL9/MIG and CXCL10/IP‐10 production in both the periphery and lymph nodes of infected animals compared with naïve controls. Animals with higher viral loads had higher levels of CXCL9/MIG and CXCL10/IP‐10 producing cells compared with animals with low viral loads. Analysis of cells bearing the receptor (CXCR3) for CXCL9/MIG and CXCL10/IP‐10 revealed increased number of CXCR3 + cells in the lymph nodes of infected animals. Importantly, an inverse correlation ( P  < 0.05) between CXCL9/MIG and CXCL10/IP‐10 production, both in the periphery and lymph nodes, and peripheral CD4 + T‐cell numbers was observed. These findings provide further evidence that dysregulation of Th1 agonist chemokines might contribute to the ultimate immunopathology during AIDS.

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