Quantification of C3 and C4 in Infertile Men with Antisperm Antibody in Their Seminal Plasma

Rahimi, Azita; Sepehri, Houri; Pakravesh, Jalil; Bahar, Kamal

doi:10.1111/j.1600-0897.1999.tb00446.x

Cited by 17 publications

(14 citation statements)

References 20 publications

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“…The role of complement in semen was strongly suggested by the observation that infection with HIV added to heated or EDTA-treated semen was no different from that seen with HIV alone (i.e., diluted in culture medium). Complement components have been detected in all body secretions, including seminal fluid (4,5). HIV is known to activate complement in serum in the presence or the absence of Abs (12,19).…”

Section: Discussionmentioning

confidence: 99%

Opsonization of HIV-1 by Semen Complement Enhances Infection of Human Epithelial Cells

Bouhlal

Chomont

Haeffner‐Cavaillon

et al. 2002

The Journal of Immunology

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In the present study we demonstrate that both X4- and R5-tropic HIV-1 strains are able to infect the human epithelial cell line HT-29. Infection was enhanced 2-fold when HIV was added to semen before contact with the cell cultures. The enhancing effect of semen was complement dependent, as evidenced by blockage of generation of C3a/C3adesArg in semen by heat or EDTA treatment of semen and suppression of semen-dependent enhancement with mAbs directed to complement receptor type 3 (CD11b/CD18) and soluble CD16. Infection of HT-29 cells was assessed by the release of p24 Ag in cultures and semiquantitative PCR of the HIV-1 pol gene. Inhibition of infection of HT-29 by stromal cell-derived factor 1 was decreased in the case of semen-opsonized X4- and R5-tropic virus compared with unopsonized virus. In contrast, inhibition of infection by RANTES was increased for opsonized X4-tropic HIV-1 compared with unopsonized virus. Taken together these observations indicate that activation of complement in semen may play an enhancing role in mucosal transmission of HIV-1 by facilitating infection of epithelial cells and/or enhancing infection of complement receptor-expressing target cells in the mucosa.

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Section: Discussionmentioning

confidence: 99%

Opsonization of HIV-1 by Semen Complement Enhances Infection of Human Epithelial Cells

Bouhlal

Chomont

Haeffner‐Cavaillon

et al. 2002

The Journal of Immunology

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“…The action of antibody on endothelial cells in the absence of complement activation also may have a role in allograft rejection, particularly chronic allograft rejection (50). Even in the absence of complement, endothelial cells demonstrate activation and proliferation in the presence of MHC class I antibodies in vitro (51,52).…”

Section: Antibody Action Without Complementmentioning

confidence: 99%

Mechanisms and Role of HLA and non-HLA Alloantibodies

Tinckam

Chandraker²

2006

Clinical Journal of the American Society of Nephrology

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The role of alloantibodies against HLA and non-HLA targets is becoming increasingly recognized as critical in the pathogenesis of acute and chronic renal allograft outcomes. This review discusses the antigenic targets, the mechanisms of T and B cell activation that result in the production of antibody, the complement cascade, methods of antibody detection, and the evidence that alloantibody-mediated mechanisms are active in acute and chronic rejection.

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“…Semen, cervicovaginal secretions, and breast milk contain complement proteins that may allow viral particles to be opsonized (3)(4)(5). Opsonization of HIV-1 with complement results in enhancement of viral infection of T and B cell lines (6,7), primary PBMC (8), and primary monocytes/ macrophages (9).…”

mentioning

confidence: 99%

Opsonization of HIV with Complement Enhances Infection of Dendritic Cells and Viral Transfer to CD4 T Cells in a CR3 and DC-SIGN-Dependent Manner

Bouhlal

Chomont

Requena

et al. 2007

The Journal of Immunology

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In the present study, we demonstrated that opsonization of primary HIV-1 with human complement enhances infection of immature monocyte-derived dendritic cells (iDC) and transmission in trans of HIV to autologous CD4+ T lymphocytes. Infection of iDC by opsonized primary R5- and X4-tropic HIV was increased 3- to 5-fold as compared with infection by the corresponding unopsonized HIV. Enhancement of infection was dependent on CR3 as demonstrated by inhibition induced by blocking Abs. The interaction of HIV with CCR5 and CXCR4 on iDC was affected by opsonization. Indeed, stromal-derived factor-1 was more efficient in inhibiting infection of iDC with opsonized R5-tropic HIV-1BaL (45%) than with heat-inactivated complement opsonized virus and similarly RANTES inhibited more efficiently infection of iDC with opsonized X4-tropic HIV-1NDK (42%) than with heat-inactivated complement opsonized virus. We also showed that attachment of complement-opsonized virus to DC-specific ICAM-grabbing nonintegrin (DC-SIGN) molecule on iDC and HeLa DC-SIGN+ CR3− cells was 46% and 50% higher compared with heat-inactivated complement opsonized virus, respectively. Hence, Abs to DC-SIGN suppressed up to 80% and 60% the binding of opsonized virus to HeLa cells and iDC, respectively. Furthermore, Abs to DC-SIGN inhibited up to 70% of the infection of iDC and up to 65% of infection in trans of autologous lymphocytes with opsonized virus. These results further demonstrated the role of DC-SIGN in complement opsonized virus uptake and infection. Thus, the virus uses complement to its advantage to facilitate early steps leading to infection following mucosal transmission of HIV.

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Quantification of C3 and C4 in Infertile Men with Antisperm Antibody in Their Seminal Plasma

Cited by 17 publications

References 20 publications

Opsonization of HIV-1 by Semen Complement Enhances Infection of Human Epithelial Cells

Opsonization of HIV-1 by Semen Complement Enhances Infection of Human Epithelial Cells

Mechanisms and Role of HLA and non-HLA Alloantibodies

Opsonization of HIV with Complement Enhances Infection of Dendritic Cells and Viral Transfer to CD4 T Cells in a CR3 and DC-SIGN-Dependent Manner

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