Mechanism of transfer of immune complexes from red blood cell CR1 to monocytes

Emlen, Woodruff; Carl, Virginia S.; Burdick, G

doi:10.1111/j.1365-2249.1992.tb06869.x

Cited by 49 publications

(41 citation statements)

References 36 publications

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“…Some studies have suggested that the transfer reaction requires Fc recognition of erythrocyte-bound complexes by fixed tissue macrophages, followed by proteolysis of CR1 (32,37). Still other studies have suggested that the transfer of soluble immune complexes from erythrocytes to monocytes is driven by the greater number of immune complex binding sites available on monocytes relative to erythrocytes and that the transfer reaction is not dependent on factor I or other enzymatic processing of immune complexes (20).…”

Section: Discussionmentioning

confidence: 99%

Antibody to the Type 3 Capsule Facilitates Immune Adherence of Pneumococci to Erythrocytes and Augments Their Transfer to Macrophages

Li¹,

Szalai²,

Hollingshead³

et al. 2009

Infect Immun

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Streptococcus pneumoniae has been shown to bind to erythrocytes via a process called immune adherence. This adherence and the subsequent transfer of pneumococci from erythrocytes to macrophages are both dependent on complement C3 deposition onto the pneumococcal surface. The observation that anti-capsule antibody increases C3 deposition on the pneumococcal capsule indicated that anti-capsule antibody may also facilitate the clearance of pneumococci through immune adherence. Using pneumococcal strain WU2 (capsule type 3) and its nonencapsulated mutant JD908, we found that monoclonal antibody (MAb) to type 3 capsule increases complement C3, C1q, and C4 deposition on WU2 and enhanced the immune adherence of WU2 to erythrocytes. The MAb to type 3 capsule also enhanced the transfer of WU2 from erythrocytes to macrophages. Moreover, the transfer reaction was inhibited by preincubating macrophages with anti-CR3 or anti-Fc␥RIII/II MAb, indicating that CR3 and Fc␥RIII/II on macrophages mediate this process. The transfer reactions of JD908 (opsonized with complement) and WU2 (opsonized with complement plus MAb to type 3 capsule) were similarly inhibited by anti-CR3 MAb, but only the latter was inhibited by anti-Fc␥RIII/II MAb. This finding indicates that although complement and the macrophage receptor CR3 are essential for the transfer reaction, if antibody is present it can further enhance the transfer reaction through a process dependent on Fc␥RIII/II. Using pre-and postvaccination sera of people immunized with the 23-valent pneumococcal polysaccharide vaccine, we confirmed that human anti-capsule antibodies are also able to increase the immune adherence of pneumococci and their transfer to macrophages.

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Section: Discussionmentioning

confidence: 99%

Antibody to the Type 3 Capsule Facilitates Immune Adherence of Pneumococci to Erythrocytes and Augments Their Transfer to Macrophages

Li¹,

Szalai²,

Hollingshead³

et al. 2009

Infect Immun

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show abstract

“…The requirement of factors H and I to cleave C3b into iC3b and hence unload the immune complexes from erythrocytes has been questioned by previous studies (12,13,24). In our experiments, transfer reactions were conducted with erythrocyte-bound pneumococci and J774A.1 macrophages in the absence of serum.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that CR1 and Fc receptors on phagocytic cells are involved in the transfer reaction of immune complexes (13,39) and that CR3 and CR4 might participate in the clearance of immune complexes. The newly described macrophage receptors CRIg and SIGN-R1 are thought to be critical in the clearance of blood-borne pathogens.…”

Section: Discussionmentioning

confidence: 99%

PspA and PspC Minimize Immune Adherence and Transfer of Pneumococci from Erythrocytes to Macrophages through Their Effects on Complement Activation

Li¹,

Glover²,

Szalai³

et al. 2007

Infect Immun

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Pneumococcal surface protein A (PspA) and PspC are important virulence factors. Their absence has been shown to allow improved clearance of pneumococci from the blood of mice and to decrease pneumococcal virulence. In the presence of antibody and complement, pneumococci attach to erythrocytes in a process called immune adherence (IA), which facilitates their delivery to, and eventual phagocytosis by, macrophages. It is not known, however, if PspA and PspC affect IA. Using PspA and/or PspC isogenic mutants and complementdeficient mouse sera, we demonstrated that absence of PspA allows greater deposition of C1q and thus increased classical-pathway-mediated C3 deposition. In the absence of both PspA and PspC, there is also a major increase in C1q-independent C3 deposition through the alternative pathway. The latter was observed even though absence of PspC alone did not have a major effect on alternative-pathway-dependent complement deposition. The enhanced complement C3 deposition realized in the absence of PspA alone and in the absence of PspA and PspC resulted in both greatly increased IA to human erythrocytes and improved transfer of pneumococci from erythrocytes to phagocytes. These data provide new insight into how PspA and PspC act in synergy to protect pneumococci from complement-dependent clearance during invasive infection.

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“…However, the precise cellular mechanisms involved in the transfer of RBC-bound ICs from RBCs to macrophages or phagocytic cells and the generation of CD235 ϩ MPs during this process remain to be elucidated. The transfer mechanism could be driven by a higher number of CR1 copies on the monocyte than on the RBCs (63) or by the close juxtaposition of the macrophage to the RBC-bound ICs that leads to macrophageassociated protease cleavage of CR1 and a release of the IC from the RBC (64). It is possible that instability of RBC membranes may occur during transfer of CR1-bound ICs from erythrocytes to acceptor phagocytic cells via Fc receptors (64,65) and thus trigger RBCs to shed MPs.…”

Section: Cd235mentioning

confidence: 99%

Microparticles Provide a Novel Biomarker To Predict Severe Clinical Outcomes of Dengue Virus Infection

Punyadee

Mairiang

Thiemmeca

et al. 2015

J Virol

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Shedding of microparticles (MPs) is a consequence of apoptotic cell death and cellular activation. Low levels of circulating MPs in blood help maintain homeostasis, whereas increased MP generation is linked to many pathological conditions. Herein, we investigated the role of MPs in dengue virus (DENV) infection. Infection of various susceptible cells by DENV led to apoptotic death and MP release. These MPs harbored a viral envelope protein and a nonstructural protein 1 (NS1) on their surfaces. Ex vivo analysis of clinical specimens from patients with infections of different degrees of severity at multiple time points revealed that MPs generated from erythrocytes and platelets are two major MP populations in the circulation of DENV-infected patients. Elevated levels of red blood cell-derived MPs (RMPs) directly correlated with DENV disease severity, whereas a significant decrease in platelet-derived MPs was associated with a bleeding tendency. Removal by mononuclear cells of complement-opsonized NS1-anti-NS1 immune complexes bound to erythrocytes via complement receptor type 1 triggered MP shedding in vitro, a process that could explain the increased levels of RMPs in severe dengue. These findings point to the multiple roles of MPs in dengue pathogenesis. They offer a potential novel biomarker candidate capable of differentiating dengue fever from the more serious dengue hemorrhagic fever. IMPORTANCEDengue is the most important mosquito-transmitted viral disease in the world. No vaccines or specific treatments are available. Rapid diagnosis and immediate treatment are the keys to achieve a positive outcome. Dengue virus (DENV) infection, like some other medical conditions, changes the level and composition of microparticles (MPs), tiny bag-like structures which are normally present at low levels in the blood of healthy individuals. This study investigated how MPs in culture and patients' blood are changed in response to DENV infection. Infection of cells led to programmed cell death and MP release. In patients' blood, the majority of MPs originated from red blood cells and platelets. Decreased platelet-derived MPs were associated with a bleeding tendency, while increased levels of red blood cell-derived MPs (RMPs) correlated with more severe disease. Importantly, the level of RMPs during the early acute phase could serve as a biomarker to identify patients with potentially severe disease who require immediate care. E ach year, up to 390 million people are infected by dengue virus (DENV), the most significant mosquito-borne virus of the Flaviviridae family, posing serious socioeconomic and health burdens globally (1). Four serotypes of viruses (DENV serotype 1 [DENV-1], DENV-2, DENV-3, and DENV-4) are transmitted to humans by Aedes mosquitoes to establish both endemic and epidemic transmission cycles primarily in tropical and subtropical countries (1). Although the majority of DENV infections in humans are subclinical, a small fraction of infected individuals develops clinical symptoms ranging from a self-...

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Mechanism of transfer of immune complexes from red blood cell CR1 to monocytes

Cited by 49 publications

References 36 publications

Antibody to the Type 3 Capsule Facilitates Immune Adherence of Pneumococci to Erythrocytes and Augments Their Transfer to Macrophages

Antibody to the Type 3 Capsule Facilitates Immune Adherence of Pneumococci to Erythrocytes and Augments Their Transfer to Macrophages

PspA and PspC Minimize Immune Adherence and Transfer of Pneumococci from Erythrocytes to Macrophages through Their Effects on Complement Activation

Microparticles Provide a Novel Biomarker To Predict Severe Clinical Outcomes of Dengue Virus Infection

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