Effect of Human Immunodeficiency Virus on Dendritic Cells Isolated from Human Peripheral Blood

Knight, Stella C.; Patterson, Steven

doi:10.1007/978-3-662-39946-0_146

Cited by 3 publications

(1 citation statement)

References 10 publications

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“…Such localization of HIV-1 in lymphoid organs could contribute to virus spread by facilitating the infection of CD4+ T cells migrating to lymphoid organs in response to infection [43][44][45]. It might also facilitate the infection of some resident FDC which co-express CD4 [46] and CR2 [27]. These hypotheses are consistent with previous results identifying lymphoid organs as major reservoirs for HIV-1 [47][48][49], and as sites of active HIV-1 replication late in the course of disease [50].…”

Section: Discussionmentioning

confidence: 99%

CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody

Montefiori

Zhou

Shaff

1992

Clinical and Experimental Immunology

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SUMMARYComplement and antibody contribute to infection-enhancement and possible expanded cellular tropism of HI V-1 in vitro through a process requiring complement receptors. Until now, however, the ability of HIV-1 to bind complement receptors has not been documented or characterized. We investigated whether antibody and complement permitted HIV-1 to bind to the B lymphocyte receptor, CR2 (CD21), in an effort to learn more about infection-enhancement, and also because CR2 can mediate B cell proliferation and antigen localization in lymphoid organs in other systems. HIV-1 incubated with antibody and fresh human serum as a source of complement bound approximately 10-fold greater to cells expressing CR2 than to HIV-1-permissive cells lacking this receptor. A similar effect was observed using cells which expressed CR2 but no CD4. This binding was minimal in heat-inactivated and C3-deficient sera, and was significantly reduced by the anti-CR2 MoAb, OICB7, but not by the anti-CD4 MoAb, OKT4a. Thus, complement and antibody acted in concert to facilitate the binding of HIV-1 to CR2 independently of CD4. CD4-independent binding of HIV-1 to CR2 was not sufficient to produce infection in Raji-3 cells. Titres of antibodies mediating CR2 binding correlated with antibody titres as measured by immunofluorescenee (/'<001) and infection-enhancement (f <005) but were discordant with titres of neutralizing antibodies, a result consistent with the utilization of CR2 for enhanced infection of cells. The ability of complement and antibody to facilitate the binding of HIV-1 to CR2 in the absence of CD4 provides new insights into mechanisms of HIV-1-induced immunopathogenesis and infection-enhancement.

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Section: Discussionmentioning

confidence: 99%

CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody

Montefiori

Zhou

Shaff

1992

Clinical and Experimental Immunology

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Antigen presentation in HIV infection

Knight¹,

Macatonia²,

Patterson³

1992

Immunology of HIV Infection

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Constitutive Expression of Major Histocompatibility Complex Class II Antigens on Monocytes and B Cells Correlates with Disease in Simian Immunodeficiency Virus-Infected Rhesus Macaques

Ashworth

Hall

Sharpe

et al. 1995

Journal of Infectious Diseases

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Constitutive host factors that influence progression to AIDS are understood poorly. In the macaque model for AIDS, 35 animals infected with simian immunodeficiency virus (SIV) were analyzed for major histocompatibility complex class II antigen expression on blood monocytes and B cells by immunostaining and flow cytometry. Expression varied widely between animals but was constant with time. Level of expression and the proportion of monocytes and B cells that expressed class II were not affected by SIV infection. Significantly more animals developed AIDS in the group with low class II expression than in the group with high expression (P < .001). Progression to disease was faster in animals that expressed poorly (P < .01), and opportunistic pathogens were more common (P < .05). Thus, the constitutive level of class II antigen expression may be a useful prognostic indicator for human immunodeficiency virus disease in humans and may be an important factor in the design of vaccine trials.

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Effect of Human Immunodeficiency Virus on Dendritic Cells Isolated from Human Peripheral Blood

Cited by 3 publications

References 10 publications

CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody

CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody

Antigen presentation in HIV infection

Constitutive Expression of Major Histocompatibility Complex Class II Antigens on Monocytes and B Cells Correlates with Disease in Simian Immunodeficiency Virus-Infected Rhesus Macaques

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