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Chapter 9 : Innate Immune Responses in HIV Infection

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Innate Immune Responses in HIV Infection, Page 1 of 2

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Abstract:

The role of various innate immune cells and soluble factors in HIV infection is covered in this chapter. The innate immune system recognizes incoming pathogens through pattern recognition receptors (PRRs). Among these are Toll-like receptors (TLRs), nucleotidebinding oligomerization domain (NOD)-like receptors (NLRs), and RIG-1-like receptors (RLRs). C-type lectin-like receptors (CLRs) also interact with carbohydrate containing organisms. Dendritic cells (DCs) DCs in the blood are the myeloid dendritic cells (MDCs) and plasmacytoid dendritic cells (PDCs). The majority of DCs are MDCs. PDCs represent <1% of the blood DCs. HIV infects DCs and usually shows low-level virus replication. MDCs are more susceptible than PDCs to virus infection and replication. The DCs can pass infectious virus to CD4 cells. Natural killer (NK) cells function through the interaction of cell surface inhibitory or activating molecules. They respond against virus-infected cells having decreased MHC class I expression. γ δ T cells differ from the conventional α β T cells in that their T-cell receptor is encoded by different gene segments. These cells, which can be infected by HIV, are present in several body tissues, but particularly in mucosae. Like NK and NK-T cells, γ δ T cells have effector functions, including cytotoxic activity and cytokine production. Innate immunity plays a role in controlling HIV infection in the central nervous system. HIV has many interactions with the innate immune system and affects immune cell number and function as well as the production of innate cytokines and soluble components.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09

Key Concept Ranking

Innate Immune System
0.66678745
Adaptive Immune System
0.6397121
Complement System
0.5935975
MHC Class I
0.48656523
0.66678745
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Figures

Image of Figure 9.1
Figure 9.1

Interaction of the innate and adaptive immune systems. Following acute infection by a microorganism, the components of the innate immune system respond rapidly, releasing cytokines that induce fever and initiating antimicrobial activity by innate immune cells (e.g., neutrophils and natural killer cells). The cytokines and the antimicrobial activity also elicit the subsequent responses of T and B cells of the adaptive immune system. Thus, a close interaction between the innate and adaptive immune systems exists, and the early activity of innate immune cells can have influence on both innate and adaptive immune responses. Adapted from reference 2528 with permission from Elsevier.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.2
Figure 9.2

Dendritic cells, uninfected and infected with HIV-1. (A) Purified dendritic cells were obtained from PBMC cultured for 6 days in GM-CSF and TNF-α. Magnification, x9,000. (B) CD4 cord blood cells were cultured with GM-CSF, TNF-α, and stem cell factor. After 7 days, the derived cells were infected with HIV-1, washed, and cultured for a further 8 days. A mature dendritic cell with a very indented nucleus and HIV on the surface (arrowhead) is shown. Magnification, x4,500. (C) Further magnification of the dendritic cell in panel B, showing HIV-1 particles on the cell surface. Magnification, x60,000. All panels provided by S. Knight and R. English.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.3
Figure 9.3

T-lymphocyte surface markers and their corresponding ligands on the antigen-presenting cell. Cell-to-cell contact between a CD8 (MHC class I-restricted) or a CD4(MHC class II-restricted) T lymphocyte and an APC involves the binding of several surface molecules with their specific ligands on the APC surface. Figure provided by S. Stranford.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.4
Figure 9.4

Morphology of PDCs and MDCs. By electron microscopy (a), PDCs appear as lymphoblasts with a medium to large diameter; a lightly eccentric, indented, round or oval nucleus; lightly stained perinuclear areas; and well developed rough endoplasmic reticulum. By scanning electron microscopy, resting PDCs have a spherical shape (b), whereas CD40L-activated PDCs have a dendritic cell-like morphology (c). Original magnifications, ×7,000 (a) and ×3,000 (b, c). By Giemsa staining, the PDC have a plasmacytoid morphology (d). The CD11c blood MDCs display dendrites by Giemsa staining (e) and electron microscopy (f). Reproduced from references 1642 and 4133 with permission.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.5
Figure 9.5

Relationship of plasmacytoid dendritic cell (PDC) number to clinical state. Each circle represents a value for a different study subject. Horizontal bars indicate the median. The number of blood PDCs is increased in long-term survivors (LTS) (< 0.05 for all group comparisons versus LTS) and decreased in AIDS patients (< 0.01 for all group comparisons versus AIDS). Most of the progressors had received antiretroviral therapy for several months; no substantial difference in PDC number was observed between these subjects and those who were untreated. Reprinted from reference 4215 with permission.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.6
Figure 9.6

Regulation of NK cell activation and function during viral infections. Soon after many acute viral infections, IFN-α/β is induced by infected cells to activate NK cell-mediated cytotoxicity and blastogenesis (open arrows pointing to the right in the top pathway). Some, but not all, viral infections also spontaneously elicit detectable IL-12 production (broken arrows pointing to the right in the bottom pathway). If IL-12 is present, NK cell production of IFN-γ is induced. The IFN-γ response has been conclusively shown to contribute to antiviral defense primarily by activating cell-mediated immune responses. IFN-/ acts to block or inhibit IL-12 expression and can cause a lack of detectable IL-12 during certain viral infections. This process, by reducing IFN-γ, could affect the extent of cell-mediated response induced by IFN-γ. Once T-cell responses are activated, they can then act to turn off the NK cell response. Reprinted from reference 374 with permission.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.7
Figure 9.7

Gene arrangement at the TCR-γ and TCR-δ loci of γδ T cells. Approximate location of V, (D), J, and C segments are illustrated. Pseudo-genes are indicated by empty boxes. Adapted from the International Immunogenetics Information System (http://imgt.cines.fr). Provided by D. Pauza.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Image of Figure 9.8
Figure 9.8

Functional network of innate immunity elements in the brain. Reprinted from reference 4229 with permission from Elsevier. MNGC, multinucleated giant cells.

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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References

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Tables

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Table 9.1

Components of the innate and adaptive immune systems

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.2

Comparison of immune systems

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.3

Pattern recognition receptors

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.4

Distribution of dendritic cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.5

Comparison of blood dendritic cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.6

Characteristics of dendritic cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.7

Characteristics of plasmacytoid dendritic cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.8

Roles of type 1 interferons

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.9

Effect of HIV infection on dendritic cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.10

Natural killer (NK) cell receptors and their ligands

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.11

NK cell function

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.12

Effects of HIV on NK cell function

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.13

Official and alternative nomenclatures for common TCR-γ and TCR-δ genes of γδ T cells

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.14

Potential role of complement in HIV infection

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.15

Features of innate immunity in the central nervous system

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.16

Potential role of complement in HIV neuropathogenesis

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09
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Table 9.17

Interactions of HIV with the innate immune system

Citation: Levy J. 2007. Innate Immune Responses in HIV Infection, p 209-235. In HIV and the Pathogenesis of AIDS, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555815653.ch09

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