Differential modulation of B7‐1 and B7‐2 isoform expression on human monocytes by cytokines which influence the development of T helper cell phenotype

Wd, Creery; Díaz‐Mitoma, Francisco; Filion, Lionel G.; Kumar, Ashok

doi:10.1002/eji.1830260614

Cited by 107 publications

(88 citation statements)

References 36 publications

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“…Murine macrophages from several lymphoid and non-lymphoid organs have been shown to poorly express B7 molecules, although expression can be upregulated in vitro by LPS or by interferon-gamma (IFN-g) [19,20]. In humans, resting monocytes constitutively express B7-2, whereas B7-1 expression is inducible in culture, particularly in the presence of IFN-g [21,22]. Tissue macrophages positive for both B7-1, B7-2 and CD40 have been identified in the interfollicular area of normal lymph nodes [23], but little is known concerning macrophages from other sites.…”

Section: Discussionmentioning

confidence: 99%

In situexpression of B7 and CD40 costimulatory molecules by normal human lung macrophages and epithelioid cells in tuberculoid granulomas

Stolzmann

Boussaud

Moreau

et al. 1999

Clinical and Experimental Immunology

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SUMMARYNormal alveolar macrophages (AM) are not efficient in inducing the proliferation of resting T lymphocytes, and, rather, tend to inhibit pulmonary immune responses. In contrast, epithelioid cells (EC), activated macrophages that play an essential role in the course of granulomatous responses, appear to stimulate T cell proliferation efficiently. The inability of macrophages to deliver potent costimulatory signals through the B7/CD28 and CD40/CD40L pathways could explain their weak accessory cell activity. Using MoAbs and immunohistochemical techniques, however, we found that essentially all AM in normal human lung tissue expressed B7-1, B7-2 and CD40 molecules, and most of these cells were strongly positive. Pulmonary macrophages in other compartments also expressed these costimulatory molecules; no differences in expression were observed comparing macrophages from smokers and non-smokers. Most AM recovered by bronchoalveolar lavage from normal lung segments also strongly expressed B7-1, B7-2 and CD40 molecules. In comparison, resting blood monocytes were B7-1 ¹ and only moderately positive for B7-2. Activation of monocytes with lipopolysaccharide (LPS) induced expression of these costimulatory molecules to levels similar to that of AM from the control subjects. EC in granulomatous lesions also expressed easily detectable levels of B7-1, B7-2 and CD40. T lymphocytes within and surrounding the granulomas expressed CD28, the counter-receptor for B7, and many of these T cells also expressed B7-1 and B7-2. These findings suggest that both AM and EC can deliver costimulatory signals through B7-1, B7-2 and CD40 molecules, and indicate that the impairment in accessory cell activity observed for normal AM cannot be attributed to the absence of expression of these costimulatory molecules.

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Section: Discussionmentioning

confidence: 99%

In situexpression of B7 and CD40 costimulatory molecules by normal human lung macrophages and epithelioid cells in tuberculoid granulomas

Stolzmann

Boussaud

Moreau

et al. 1999

Clinical and Experimental Immunology

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“…Spontaneous production of IL-10 by unstimulated PBMC from HIV þ individuals may also contribute to the defective antigen/recall responses and immunological unresponsiveness/immune suppression. The mechanism by which IL-10 induces immunosuppression has been attributed in part to its inhibitory effects on the synthesis of cytokines such as IL-2, IL-12 and interferon-gamma (IFN-g) [17][18][19]47] and inhibiting B7.2 expression on APC [16,48]. Increased expression of IL-10 [23,40,41] and decreased production of IL-12 by monocytes of HIV þ individuals [28,31] may induce immune unresponsiveness by inhibiting the CD28-B7 pathway, as IL-10 and IL-12 mediate their biological effects by regulating the CD28-B7 pathway [16,49].…”

Section: Discussionmentioning

confidence: 99%

Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

Kumar

Angel

Daftarian³

et al. 1998

Clinical and Experimental Immunology

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SUMMARYImmune unresponsiveness in HIV-1 infection can result from impaired signals delivered by the costimulatory CD28-B7 pathway and the altered production of immunoregulatory cytokines, in particular IL-10, whose production is altered in HIV-1 infection. In this study we investigate IL-10 regulation in T cells and monocytes from HIV þ individuals, and its association with CD28-mediated T cell proliferation. IL-10 production as analysed in T cell-and monocyte-depleted peripheral blood mononuclear cells (PBMC), and by intracellular staining at the single-cell level, reveals a defect in IL-10 production by CD4 þ and CD8 þ T cells, whereas monocytes constitute the major IL-10-producing cell type. To investigate the impact of IL-10 on immune responsiveness, CD28-mediated proliferative responses in HIV þ individuals were correlated with PHA-induced IL-10 production. CD4 þ T cells expressed CD28, yet exhibited markedly reduced CD28-mediated cell proliferation. This CD28-mediated CD4 þ T cell proliferation was found to be inversely associated with the levels of PHAinduced IL-10 production and could be restored, at least in part, by anti-IL-10 antibodies. These results suggest that IL-10 production is differentially regulated in T cells and monocytes of HIV þ individuals, and that IL-10 may have a role in inducing immune unresponsiveness by modulating the CD28-B7 pathway.

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“…is another mechanism by which CD80/CD86 expression is regulated (21,24,39,43,46,54). For instance, T lymphocytes activated through CD3/CD28 will express both CD80 and CD86 (4,14,48,56). Thus, it will be interesting to investigate the possible relationships between the types of producer cells in which HIV-1 is expanded (e.g., CD4 ϩ T cells versus macrophages), the types of stimuli used to activate virus producer cells, and the degree of incorporation of CD80 and CD86 into mature HIV-1 particles.…”

Section: Discussionmentioning

confidence: 99%

“…Efficient incorporation of CD80 and CD86 in clinical isolates of HIV-1 produced by cytokine-treated macrophages. As specified above, the two most important cellular reservoirs of HIV-1, i.e., monocytes/macrophages and CD4 ϩ T lymphocytes, can also express both CD80 and CD86 (3,4,14,24,25,48,56). Since CD80 and CD86 are upregulated after the treatment of cells of the monocytic lineage with cytokines (reviewed in reference 28), we finally studied the process of CD80 and CD86 incorporation in field isolates of HIV-1 bearing distinct coreceptor utilization profiles (i.e., R5 and X4).…”

Section: Fig 3 the Infectivity Of Cd80-and Cd86-bearing Hiv-1 Viriomentioning

confidence: 95%

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Insertion of Host-Derived Costimulatory Molecules CD80 (B7.1) and CD86 (B7.2) into Human Immunodeficiency Virus Type 1 Affects the Virus Life Cycle

Giguère

Bounou

Paquette

et al. 2004

J Virol

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Human immunodeficiency virus type 1 (HIV-1) carries virus-encoded and host-derived proteins. Recent advances in the functional characterization of host molecules inserted into mature virus particles have revealed that HIV-1 biology is influenced by the acquisition of host cell membrane components. The CD28/B7 receptor/ ligand system is considered one of the fundamental elements of the normal immune response. Two major cell types that harbor HIV-1 in vivo, i.e., monocytes/macrophages and CD4 ؉ T cells, express the costimulatory molecules CD80 (B7.1) and CD86 (B7.2). We investigated whether CD80 and CD86 are efficiently acquired by HIV-1, and if so, whether these host-encoded molecules can contribute to the virus life cycle. Here we provide the first evidence that the insertion of CD80 and CD86 into HIV-1 increases virus infectivity by facilitating the attachment and entry process due to interactions with their two natural ligands, CD28 and CTLA-4. Moreover, we demonstrate that NF-B is induced by CD80-and CD86-bearing virions when they are combined with the engagement of the T-cell receptor/CD3 complex, an event that is inhibited upon surface expression of CTLA-4. Finally, both CD80 and CD86 were found to be efficiently incorporated into R5-and X4-tropic field strains of HIV-1 expanded in cytokine-treated macrophages. Thus, besides direct interactions between the virus envelope glycoproteins and cell surface constituents, such as CD4 and some specific chemokine coreceptors, HIV-1 may attach to target cells via interactions between cell-derived molecules incorporated into virions and their natural ligands. These findings support the theory that HIV-1-associated host proteins alter virus-host dynamics.

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Differential modulation of B7‐1 and B7‐2 isoform expression on human monocytes by cytokines which influence the development of T helper cell phenotype

Cited by 107 publications

References 36 publications

In situexpression of B7 and CD40 costimulatory molecules by normal human lung macrophages and epithelioid cells in tuberculoid granulomas

In situexpression of B7 and CD40 costimulatory molecules by normal human lung macrophages and epithelioid cells in tuberculoid granulomas

Differential production of IL-10 by T cells and monocytes of HIV-infected individuals: association of IL-10 production with CD28-mediated immune responsiveness

Insertion of Host-Derived Costimulatory Molecules CD80 (B7.1) and CD86 (B7.2) into Human Immunodeficiency Virus Type 1 Affects the Virus Life Cycle

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