Anti-Cd2 and Anti-Cd3 Monoclonal Antibodies Synergize to Prolong Allograft Survival With Decreased Side Effects

Chavin, Kenneth D.; Qin, Lihui; Lin, Jixun; Kaplan, Adam J.; Bromberg, Jonathan S.

doi:10.1097/00007890-199304000-00040

Cited by 31 publications

(17 citation statements)

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“…2C), CBA/J splenocytes were cultured in MLR with histoincompatible C57BL/6 stimulators, and various combinations of anti-CD2 and/or anti-CD62L mAbs were added at the initiation of culture. As expected, anti-CD2 mAb had a small inhibitory effect on the MLR response (25,27). Anti-CD62L mAb alone, or in combination with anti-CD2 mAb, had no additional effect on the MLR.…”

Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costisupporting

confidence: 68%

“…The administration of anti-CD2 plus anti-CD3 mAbs resulted in prolonged allograft survival for all recipients and tolerance (Fig. 1A, and data not shown) (25). If anti-CD62L mAbs were added to the tolerogenic regimen of anti-CD2 plus anti-CD3 mAbs, mean survival time was only 37 Ϯ 4.1 days, showing that prolonged graft survival and tolerance were prevented.…”

Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costimentioning

confidence: 82%

“…Naive splenic lymphocytes were stimulated in culture with anti-CD3, anti-CD2, anti-CD62L, or control mAbs singly or in combination. Anti-CD3 mAbs (1 or 0.1 g/ml) induced substantial proliferation that could be partly inhibited by anti-CD2 mAb (25,27,29) (Fig. 2A).…”

Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costimentioning

confidence: 92%

“…Donor neonatal (P1-2) C3H or C57BL/6 mice were sacrificed, and whole hearts were removed and placed in a s.c. pocket in the ear pinnae of recipients (25). The survival of the allografts was followed by EKG (Powerlab Software Installer, AD Instruments, Mountain View, CA) every other day.…”

Section: Nonvascularized Cardiac Transplantationmentioning

confidence: 99%

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L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

Bai

Liu

Wang

et al. 2002

The Journal of Immunology

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Maneuvers that interfere with signals 1, 2, 3, or Ag processing can result in indefinite allograft survival. However, they are not applicable to all tissues, strains, or species, suggesting that there are additional levels of immune regulation. We hypothesized that secondary lymphoid organs are important for interactions among lymphocytes, alloantigen, and immunosuppressants that lead to tolerance. To explore this, cardiac allografts were performed with a tolerogenic immunosuppressive regimen. Concurrent administration of anti-L-selectin (CD62L) Ab, which prevents lymph node homing, prevents indefinite allograft survival and tolerance. Anti-CD62L Ab is not costimulatory, and Fab and F(ab′)2 anti-CD62L have similar activities. Flow cytometry and histologic examination show that Ab shifts T cells away from lymph nodes and into spleen, peripheral blood, and graft. Tolerance is not induced in CD62L−/− mice, and adoptive transfer of CD62L−/−, but not CD62L+/+, T cells prevents tolerization in wild-type recipients. FTY720, an immunosuppressant that promotes chemokine-dependent, but CD62L-independent, lymph node homing, reverses the Ab effect. Blockade of other homing receptors also prevents tolerization. These results indicate that T lymphocytes use CD62L-dependent migration for alloantigen-specific tolerance, and suggest that lymph nodes or other lymphoid tissues are an important site for peripheral tolerization to alloantigen.

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Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costisupporting

confidence: 68%

Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costimentioning

confidence: 82%

Section: Anti-cd62l Mab Prevents Tolerance Induction and Has No Costimentioning

confidence: 92%

Section: Nonvascularized Cardiac Transplantationmentioning

confidence: 99%

See 2 more Smart Citations

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

Bai

Liu

Wang

et al. 2002

The Journal of Immunology

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“…The virus can be lymphocyte chemotactic response, inducing a chemokinedependent homing and sequestration of lymphocytes in secondary lymphoid organs, and preventing lymphocytes from migrating to graft sites (35). Anti-CD3 mAb inhibits antigenreceptor-driven T-cell activation and prolongs allograft survival (36). When FIV-vIL-10 was used in combination with anti-CD40L mAb or anti-CD3 mAb, the mean survival was prolonged to 27 AE 4.6 days or 45.5 AE 4.9 days, respectively, much longer than with each immunosuppressive alone.…”

Section: Discussionmentioning

confidence: 99%

Feline Immunodeficiency Virus-Mediated Viral Interleukin-10 Gene Transfer Prolongs Non-Vascularized Cardiac Allograft Survival

Chen

Mao

et al. 2003

American Journal of Transplantation

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Previous experiments demonstrated plasmid‐, retroviral‐, or adenoviral‐mediated vIL‐10 gene transfer could prolong allograft survival, but transgene expression was rapidly extinguished. Feline immunodeficiency virus (FIV) can integrate into genomic DNA of nondividing cells, resulting in indefinite transgene expression. We hypothesized FIV‐mediated gene transfer could provide long‐term gene expression, and improved allograft survival. FIV‐vIL‐10 and FIV‐β‐gal were produced using the FELIX vector system. With vector transfer to syngeneic cardiac grafts, β‐galactosidase reporter gene expression was noted as early as day 5, was strongly expressed at days 10 and 20, and persisted for 50 days after transplantation. For allografts, FIV‐vIL‐10 gene transfer more than doubled mean survival from 10 ± 1.6 to 22.3 ± 3 days. When combined with other immunosuppressants, such as anti‐CD40L mAb, FTY720, or anti‐CD3 mAb, the mean survival times were prolonged to 27 ± 4.6 days, 27.8 ± 4.6 days, and 45.5 ± 4.9 days, respectively. Multiple chemokine and chemokine receptor genes were induced by ischemia‐reperfusion injury in syngeneic grafts, and in allogeneic grafts more genes were induced and to a greater degree. In allogeneic grafts transduced with FIV‐IL‐10, a number of the chemokine genes were suppressed. Therefore, FIV virus‐mediated vIL‐10 gene transfer prolongs allograft survival and, in combination with other agents, produces an additive effect.

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Treatment of rat hemiparkinson model with xenogeneic neural transplantation: Tolerance induction by anti-T-cell antibodies

Okura¹,

Tanaka²,

Ono³

et al. 1997

J. Neurosci. Res.

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To obtain basic knowledge for the application of xenogeneic neural transplantation to patients with Parkinson's disease, the rejection process of xenogeneic neural grafts in rats was examined and a therapy to control it was developed. Tissues including the ventral mesencephalon were taken from mouse embryos and transplanted into the right lateral ventricle of mature male rats. Transplanted xenografts were usually rejected by day 15. To prevent the graft rejection, host rats were treated with anti-T-cell receptor alphabeta (anti-TCR alphabeta) or anti-CD2 monoclonal antibody (mAb) or by a combination of the two. Anti-TCR alphabeta (1 mg/kg) and anti-CD2 (7 mg/kg) mAb were administered for 3 consecutive days (day -2, -1, and 0 of transplantation). Although the administration of mAb against either CD2 or TCR alphabeta did not induce tolerance, the combination therapy with anti-CD2 and anti-TCR alphabeta mAb produced graft survival for more than 100 days. The tolerance induced by this combined antibody therapy is antigen specific because rats with long-term surviving neural xenograft accepted a second neural graft from the same donor strain C3H/He mouse, but not from a third-party strain BALB/c mouse, without additional treatment. In addition, T cells isolated from these rats did not respond to cultured C3H/He brain cells, but did respond vigorously to BALB/c brain cells in mixed lymphocyte reaction. More importantly, the finding that xenograft transplantation with the proper treatment reduced the rotation rate of 6-OHDA-lesioned rats confirmed that surviving grafts functioned properly. The results of the present study suggest that xenogeneic neural transplantation in combination with T-cell-targeted immunotherapy is an effective approach for treatment of Parkinson's disease.

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Anti-Cd2 and Anti-Cd3 Monoclonal Antibodies Synergize to Prolong Allograft Survival With Decreased Side Effects

Cited by 31 publications

References 0 publications

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

L-Selectin-Dependent Lymphoid Occupancy Is Required to Induce Alloantigen-Specific Tolerance

Feline Immunodeficiency Virus-Mediated Viral Interleukin-10 Gene Transfer Prolongs Non-Vascularized Cardiac Allograft Survival

Treatment of rat hemiparkinson model with xenogeneic neural transplantation: Tolerance induction by anti-T-cell antibodies

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