Abstract:
:Antiretroviral therapy (ART) is a life-saving intervention in human immunodeficiency virus (HIV) infection. Immune restoration after ART dramatically reduces the incidence and severity of opportunistic diseases and death. On some occasions, immune restoration may be erratic, leading to acute inflammatory responses (known as immune reconstitution inflammatory syndrome) shortly after ART initiation, or incomplete, with residual inflammation despite chronic treatment, leading to non-infectious morbidity and mortality. We propose that ART may not always restore the perfect balance of innate and adaptive immunity in strategic milieus, predisposing HIV-infected persons to complications of acute or chronic inflammation. The best current strategy for fully successful immune restoration is early antiretroviral therapy, which can prevent acquired immunodeficiency syndrome (AIDS)-associated events, restrict cell subset imbalances and dysfunction, while preserving structural integrity of lymphoid tissues. Future HIV research should capitalize on innovative techniques and move beyond the static study of T-cell subsets in peripheral blood or isolated tissues. Improved targeted therapeutic strategies could stem from a better understanding of how HIV perturbs the environmental niches and the mobility and trafficking of cells that affect the dynamic cell-to-cell interactions and determine the outcome of innate and adaptive immune responses.
journal_name
Immunol Revjournal_title
Immunological reviewsauthors
Wilson EM,Sereti Idoi
10.1111/imr.12064subject
Has Abstractpub_date
2013-07-01 00:00:00pages
343-54issue
1eissn
0105-2896issn
1600-065Xjournal_volume
254pub_type
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journal_title:Immunological reviews
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journal_title:Immunological reviews
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journal_title:Immunological reviews
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更新日期:2011-09-01 00:00:00
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journal_title:Immunological reviews
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更新日期:2009-11-01 00:00:00
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journal_title:Immunological reviews
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journal_title:Immunological reviews
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abstract::Mutations of the genes encoding T-cell receptor (TCR)-proximal signaling molecules, such as ZAP-70, can be causative of immunological diseases ranging from T-cell immunodeficiency to T-cell-mediated autoimmune disease. For example, SKG mice, which carry a hypomorphic point mutation of the Zap-70 gene, spontaneously de...
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journal_title:Immunological reviews
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