Mac-1 (CD11b/CD18) is crucial for effective Fc receptor–mediated immunity to melanoma

Mac-1 (CD11b/CD18) is crucial for effective Fc receptor–mediated immunity to melanoma

Antibody-reliant destruction of tumor cells by immune effector cells is mediated by antibody-dependent cellular cytotoxicity, in which Fc receptor (FcR) engagement is crucial. This study documents an important role for the β2 integrin Mac-1 (CD11b/CD18) in FcR-mediated protection against melanoma. C...

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Bibliographic Details
Published in:Blood Vol. 101; no. 1; pp. 253 - 258
Main Authors: van Spriel, Annemiek B., van Ojik, Heidi H., Bakker, Annie, Jansen, MarcoJ.H., van de Winkel, JanG.J.
Format: Journal Article
Language:English
Published: Washington, DC Elsevier Inc 01-01-2003
The Americain Society of Hematology
Subjects:
Animals
Antibodies, Neoplasm
Antibody Formation
Biological and medical sciences
CD11b Antigen - genetics
CD11b Antigen - immunology
Chemotaxis, Leukocyte
Granulocyte Colony-Stimulating Factor - pharmacology
Host-tumor relations. Immunology. Biological markers
Lung Neoplasms - secondary
Macrophage-1 Antigen - genetics
Macrophage-1 Antigen - immunology
Medical sciences
Melanoma - immunology
Melanoma - pathology
Mice
Mice, Knockout
Neutrophils - cytology
Receptors, Fc - immunology
Tumors
Antineoplastic agent
Immune response
Rodentia
Cell adhesion molecule
Immunoglobulin receptor
Cytotoxicity
Malignant tumor
Vertebrata
Mammalia
Mouse
Animal
Antibody-dependent cell cytotoxicity
Malignant melanoma
β2 integrin
Biological receptor
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Summary:Antibody-reliant destruction of tumor cells by immune effector cells is mediated by antibody-dependent cellular cytotoxicity, in which Fc receptor (FcR) engagement is crucial. This study documents an important role for the β2 integrin Mac-1 (CD11b/CD18) in FcR-mediated protection against melanoma. CD11b-deficient mice, those that lack Mac-1, were less protected by melanoma-specific monoclonal antibody TA99 than wild-type (WT) mice. Significantly more lung metastases and higher tumor loads were observed in Mac-1−/− mice. Histologic analyses revealed no differences in neutrophil infiltration of lung tumors between Mac-1−/− and WT mice. Importantly, Mac-1−/−phagocytes retained the capacity to bind tumor cells, implying that Mac-1 is essential during actual FcR-mediated cytotoxicity. In summary, this study documents Mac-1 to be required for FcR-mediated antimelanoma immunity in vivo and, furthermore, supports a role for neutrophils in melanoma rejection.
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ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V101.1.253