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Blood, 15 April 2002, Vol. 99, No. 8, pp. 2859-2868
IMMUNOBIOLOGY
Disrupted homeostasis of Langerhans cells and interdigitating
dendritic cells in monkeys with AIDS
Michael I. Zimmer,
Adriana
T. Larregina,
Cielo M. Castillo,
Saverio Capuano III,
Louis D. Falo Jr,
Michael Murphey-Corb,
Todd A. Reinhart, and
Simon M. Barratt-Boyes
From the Department of Infectious Diseases and
Microbiology, Graduate School of Public Health, and the Departments of
Dermatology, and Molecular Genetics and Biochemistry, School of
Medicine, University of Pittsburgh, PA.
Langerhans cells (LCs) are immature dendritic cells (DCs) that
capture antigen in peripheral tissues and migrate to draining lymph
nodes, where they reside in the paracortex as interdigitating dendritic
cells (IDCs). We studied the effects of simian immunodeficiency virus
(SIV) on LCs and IDCs during different stages of infection in monkeys.
LCs isolated from monkeys with acute SIV infection or acquired
immunodeficiency syndrome (AIDS) underwent normal maturation in vitro,
including a switch in chemokine receptor expression from CCR5 to CXCR4
and CCR7. LCs migrated normally from skin in response to contact
sensitization in monkeys with acute SIV infection. In contrast, LC
migration from skin was markedly impaired during AIDS, associated with
a reduction in antigen-bearing DCs in draining lymph nodes. Lymph node
IDCs were increased in proportion during acute SIV infection and had an
activated phenotype, whereas during AIDS IDCs had significantly lower
expression of CD40 and the activation marker CD83. IDCs from monkeys
with AIDS were refractory to stimulation with CD40L, demonstrating a
functional consequence of decreased CD40 expression. SIV-infected DCs
were not identified in lymph nodes or skin of monkeys with AIDS,
suggesting an indirect effect of infection on DC populations in vivo.
These data indicate that DCs are mobilized to lymph nodes during acute SIV infection, but that during AIDS this process is suppressed, with LC
migration and IDC activation being impaired. We conclude that
disruption of DC homeostasis may play a role in immunopathology induced
by human immunodeficiency virus and suggest that therapeutic strategies
targeting DCs may have limited efficacy during AIDS.
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