Receptor sites for complement and for immune complexes on human nonhemopoietic tumor cells

Biran, Haim; Mavligit, Giona M.; Moake, Joel L.

doi:10.1002/1097-0142(197907)44:1<131::aid-cncr2820440123>3.0.co;2-#

Cited by 13 publications

(3 citation statements)

References 25 publications

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“…At the same time, Isaac Witz showed the presence of IgG within non-lymphoid tumor tissue and observed that these IgG did not exhibit any antibody activity against tumor antigens, suggesting that they bound to tumor cells via their Fc region [50]. This hypothesis was supported by further experiments where primary cultures of tumors and SRBC formed rosettes [51, 52]. In addition, it was observed that tumor cells injected in mice immunized with non-tumoral antigens were able to bind antibody via their Fc region [53].…”

Section: Expression Of Tumor Fcγriibmentioning

confidence: 98%

Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity

Cohen-Solal

Cassard

Fournier

et al. 2010

Dermatology Research and Practice

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Our research, inspired by the pioneering works of Isaac Witz in the 1980s, established that 40% of human metastatic melanomas express ectopically inhibitory Fc gamma receptors (FcγRIIB), while they are detected on less than 5% of primary cutaneous melanoma and not on melanocytes. We demonstrated that these tumoral FcγRIIB act as decoy receptors that bind the Fc portion of antimelanoma IgG, which may prevent Fc recognition by the effector cells of the immune system and allow the metastatic melanoma to escape the humoral/natural immune response. The FcγRIIB is able to inhibit the ADCC (antibody dependent cell cytotoxicity) in vitro. Interestingly, the percentage of melanoma expressing the FcγRIIB is high (70%) in organs like the liver, which is rich in patrolling NK (natural killer) cells that exercise their antitumoral activity by ADCC. We found that this tumoral FcγRIIB is fully functional and that its inhibitory potential can be triggered depending on the specificity of the anti-tumor antibody with which it interacts. Together these observations elucidate how metastatic melanomas interact with and potentially evade humoral immunity and provide direction for the improvement of anti-melanoma monoclonal antibody therapy.

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Section: Expression Of Tumor Fcγriibmentioning

confidence: 98%

Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity

Cohen-Solal

Cassard

Fournier

et al. 2010

Dermatology Research and Practice

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“…Some previous reports have established that most Fe receptor-bearing cells within tumours were macrophages (Kerbel & Pross, 1976, Wood & Gollahon, 1977 and the Fe receptor has thus been caused as an index of host infiltration into the tumours (Kerbel & Pross, 1976). Other authors have claimed the presence of Fe receptors on tumour cells also (T0nder et al, 1978;Biran et al, 1979) and on a large proportion of TIL (Hayry & T0tterman, 1978;Vose et al, 1977). In malignant melanoma, the largest population of infiltrating cells were esterase-negative, non-phagocytic, non-T and non-B cells with Fc receptors (Roubin et al, 1975).…”

Section: Discussionmentioning

confidence: 96%

Cells bearing Fc receptors in human malignant solid tumours

Jl¹,

Andersson²

1982

Br J Cancer

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Summary.-Fc-receptor-bearing cells forming EA rosettes with antibody-coated human erythrocytes (Ripley) were studied in cell suspensions and in purified preparations of mononuclear cells (MC) from 20 human malignant tumours.The EA rosettes were studied in preparations made by cytocentrifugation and the rosette-forming cells identified by their nonspecific-esterase activity and phagocytic capacity.Fc receptors were found on 16+20% of all cells in the primary cell suspensions.Significantly more tumour-infiltrating lymphocytes had detectable Fc receptors (33+18%) than did peripheral-blood lymphocytes in cancer patients (19+8%) and normal control subjects (14 + 6 %). There was a significant correlation between the proportion of lymphocytes lacking T and B markers (null cells) and the proportion of lymphocytes with Fc receptors.Fc receptors were also found on most tumour-infiltrating macrophages, on some T lymphocytes and polymorphonuclear cells and on a smaller percentage of the tumour cells.The significance of the Fc receptor and its usefulness as a marker of "host infiltration" into the tumours is discussed.

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“…At the same time, Witz et al showed the presence of IgG within non-lymphoid tumor tissue and that these IgG did not exhibit any antibody activity against tumor antigens suggesting that they bound to tumor cells likely via their Fc region [39]. This hypothesis was supported by further experiments where the formation of rosettes between cells from primary cultures of tumors and SRBC was observed [40,41]. In addition, it was observed that tumor cells injected in mice immunized with non-tumoral antigens were able to bind antibody via their Fc region [42].…”

Section: Ectopic Expression Of Fcγr On Non-hematopoietic Tumor Cellsmentioning

confidence: 91%

Fc gamma receptors and cancer

Cassard

Cohen-Solal

Camilleri-Broët

et al. 2006

Springer Semin Immun

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FcgammaRs are a family of heterogeneous molecules that play opposite roles in immune response and control the effector functions of IgG antibodies. In many cancers, IgG antibodies are produced that recognize cancer cells, form immune complexes and therefore, activate FcgammaR. The therapeutic efficacy of monoclonal IgG antibodies against hematopoietic and epithelial tumors also argue for an important role of IgG antibodies in anti-tumor defenses. Since the 1980s, a series of lines of evidence in experimental models and in humans strongly suggest that FcgammaR are involved in the therapeutic activity of monoclonal IgG antibodies by activating the cytotoxic activity of FcgammaR-positive cells such as NK cells, monocytes, macrophages and neutrophils and by increasing antigen presentation by dendritic cells. Since many cell types co-express activating and inhibitory FcgammaR, the FcgammaR-dependent effector functions of IgG anti-tumor antibodies are counterbalanced by the inhibitory FcgammaRIIB. In addition, some tumor cells express FcgammaR either constitutively, such as B cell lymphomas or ectopically, such as 40% of human metastatic melanoma. The tumor FcgammaR isoform is preferentially FcgammaRIIB, which is functional at least in human metastatic melanoma. This review summarizes these data and discusses how FcgammaRIIB expression may influence the anti-tumor immune reaction and how beneficial or deleterious this expression could be for the efficiency of therapeutics based on monoclonal anti-tumor antibodies.

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Receptor sites for complement and for immune complexes on human nonhemopoietic tumor cells

Cited by 13 publications

References 25 publications

Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity

Metastatic Melanomas Express Inhibitory Low Affinity Fc Gamma Receptor and Escape Humoral Immunity

Cells bearing Fc receptors in human malignant solid tumours

Fc gamma receptors and cancer

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