MICA is a target for complement-dependent cytotoxicity with mouse monoclonal antibodies and human alloantibodies

Zou, Yizhou; Mirbaha, Fariba; Lázaro, A. M.; Zhang, Yanzheng; Lavingia, Bhavna; Šťastný, Peter

doi:10.1016/s0198-8859(01)00349-4

Cited by 68 publications

(63 citation statements)

References 9 publications

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“…In the present experiments we measured the surface expression of MICA by flow cytometry and total cellular expression by Western blot using mAbs specific for MICA (17,18). Our initial results with fibroblasts were similar to those published by others (19 -21), suggesting that the expression of surface MICA was maintained or even increased after HCMV infection.…”

supporting

confidence: 85%

“…mAbs specific for MICA, including the monomorphic Ab 6B3 (recognizing MICA native protein), the polymorphic Ab 3.2H3 (which does not react with MICA*001, but recognizes all other MICA native and denatured alleles tested), and 1.7AD (which reacts with denatured MICA protein), were produced by us as previously described (17,18). Isotype-matched, purified normal mouse IgG and anti-actin mAb (Santa Cruz Biotechnology) were used at the appropriate concentrations as a negative control in flow cytometry and as an internal positive control in Western blot.…”

Section: Monoclonal Absmentioning

confidence: 99%

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Effect of Human Cytomegalovirus on Expression of MHC Class I-Related Chains A

Zou

Bresnahan

Taylor

et al. 2005

The Journal of Immunology

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The MHC-encoded MHC class I-related chains A (MICA) glycoproteins are known to enhance the functions of NK and T cells by ligating the stimulating receptor NKG2D and appear to play an important role in host defense. Human CMV (HCMV) evades the immune response in many different ways, but has not previously been found to down-regulate MICA. We have found that a common form of MICA, which has a nucleotide insertion in exon 5 corresponding to the transmembrane region and no cytoplasmic tail, was increased on the surface of fibroblasts HFS-13 compared with the mock-infected sample of the same cells that had been cultured to confluence. However, an astrocytoma cell line, U373, which has a full-length variant of MICA, showed that the expression of MICA was decreased after HCMV infection. Retroviral transduction of different MICA alleles into fibroblasts HFF-D, which express no MICA of their own, established that full-length MICA was down-regulated by HCMV, and the truncated form was not. Fibroblasts with decreased MICA due to HCMV infection were found to be protected from NK cell killing, whereas in the presence of the truncated form of MICA, the virus-infected cells were destroyed. Thus, the truncated form of MICA, which is the most common, has a mutation that allows it to persist on the surface and hinder efforts of the virus to evade the immune response.

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supporting

confidence: 85%

Section: Monoclonal Absmentioning

confidence: 99%

Effect of Human Cytomegalovirus on Expression of MHC Class I-Related Chains A

Zou

Bresnahan

Taylor

et al. 2005

The Journal of Immunology

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“…Recent reports show that the MICA molecule may contribute to the pathogenesis of acute and chronic allograft rejection due to its expression on endothelial cells and its capacity to induce antibodies which are capable of causing complement-dependent cytotoxicity (6,7). In fact, renal and pancreatic grafts with evidence of both acute and chronic rejection have a remarkably high MICA protein expression (8), and anti-MIC antibodies (Abs) have been identified in the serum of these patients (9,10).…”

Section: Introductionmentioning

confidence: 99%

The Relationship of Anti-MICA Antibodies and MICA Expression with Heart Allograft Rejection

Suárez-Álvarez

López-Vázquez

González

et al. 2007

American Journal of Transplantation

102

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The role of MICA antibodies in acute heart allograft rejection was examined utilizing 190 pre-and posttransplant serum samples from 44 patients collected during the first year after transplantation. MICA antibodies were detected by CDC test on recombinant cell lines and by the newly developed Luminex MICA antibody detection assay. Additionally, MICA expression was analyzed by 'real time' RT-PCR and by immunohistochemistry in 10 endomyocardial biopsies. Only two subjects had HLA antibodies post-transplant. Nevertheless, MICA antibodies were found in a significant number of subjects. The prevalence of MICA antibodies was significantly higher among those with severe acute rejection (AR) than in those without rejection (60.7% vs. 14.3%, p = 0.0038 by CDC; 55.5% vs. 5.7%, p = 0.0020 by Luminex). In most cases, the appearance of MICA antibodies post-transplant precedes AR. Following transplantation, MICA up-regulation correlated with histological evidence of severe rejection. Monitoring for MICA antibodies post-transplant may be useful to establish new risk factors for acute rejection.

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“…MICA antibodies have been reported in renal and heart transplant patients whose grafts later failed, although donor specificity was not determined (4, 6). Zou et al (10) demonstrated that MICA antibodies are capable of fixing complement and killing of Hela cells in vitro suggesting these antibodies can cause complement-mediated damage of the donor endothelium. In the subset of 72 patients where we could determine MICA genotypes for the donor and recipient, we showed a significant correlation between development of DSA to donor MICA antigens and AMR.…”

Section: Discussionmentioning

confidence: 99%

“…Alloantibodies against MICA have been associated with acute and chronic vascular rejection in solid organ transplants (4 -9) and can be cytotoxic to ECs in the presence of complement (10). However, most studies reporting a role for MICA in transplantation have been indirect and circumstantial because organ donors are not routinely typed for MICA and the donor specificity of the antibodies was not ascertained.…”

Section: Introductionmentioning

confidence: 99%