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Association between decreased CXCL12 and CCL25 expression and increased apoptosis in lymphoid tissues of cynomolgus macaques during SIV infection
Author(s) -
Qin Shulin,
Sui Yongjun,
MurpheyCorb Michael A.,
Reinhart Todd A.
Publication year - 2008
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 - 10.1111/j.1600-0684.2008.00327.x
Subject(s) - chemokine , biology , apoptosis , simian immunodeficiency virus , macaque , ccl25 , immune system , lymphatic system , immunology , cytokine , chemokine receptor , paleontology , biochemistry
Background Chemokines likely play multiple roles in HIV‐1 and SIV pathogenesis. To examine potential associations between chemokine expression levels and apoptosis of cells in lymphoid tissues during SIV infection, we measured chemokine and cytokine mRNA levels in multiple lymphoid tissues compartments from uninfected and SIV‐infected cynomolgus macaques ( Macaca fascicularis ). Methods Real‐time RT‐PCR was used to measure host mRNA levels in macaque lymphoid tissues. Proliferating or apoptotic cells were identified in lymphoid tissues by immunohistochemistry. Results We found that CXCL12 and CCL25 mRNAs in SIV‐infected lymphoid tissues were decreased and their levels were negatively correlated with the numbers of proliferating and apoptotic cells. In vitro analyses revealed that CXCL12 and CCL25 were capable of reducing apoptosis induced by SIV infection. Conclusions These findings suggest that increased apoptosis in lymphoid tissues due to reduced levels of anti‐apoptotic chemokines might be a mechanism that contributes to loss of immune function following pathogenic SIV infection.