**Acknowledgements**

This work was supported by Grant 254434 from Consejo Nacional de Ciencia y Tecnología, México.

**35**

**Author details**

Carlos Rosales1

provided the original work is properly cited.

Autónoma de México, Mexico City, Mexico

and Eileen Uribe-Querol2

\*Address all correspondence to: euquerol@comunidad.unam.mx

Nacional Autónoma de México, Mexico City, Mexico

*Neutrophil Activation by Antibody Receptors DOI: http://dx.doi.org/10.5772/intechopen.80666*

© 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*

1 Immunology Department, Instituto de Investigaciones Biomédicas, Universidad

2 Advanced Research Division, Facultad de Odontología, Universidad Nacional

*Neutrophil Activation by Antibody Receptors DOI: http://dx.doi.org/10.5772/intechopen.80666*

*Neutrophils*

them.

**7. Conclusion**

**Acknowledgements**

Tecnología, México.

functions in clinical settings. For example, in intense infections, it may be important to activate phagocytosis. Because IgG2 binds better to FcγRIIa than to FcγRIIIb [33, 35], it is likely that IgG2 antibodies would activate phagocytosis by neutrophils much better than other IgG subclass antibodies. In consequence, promoting IgG2 antibodies against certain pathogens would result in better phagocytosis against

Fcγ receptors expressed in different immune cells are capable of activating different cellular responses important not only for controlling microbial infections but also for regulating immunity [71, 97]. Different subclasses of IgG antibodies bind the various Fcγ receptors with different affinities [33, 35] and can activate various cellular functions of great importance for host defense and for immune regulation. In the human neutrophil, it is clear that a specific Fcγ receptor activates particular cellular responses. FcγRIIa induces efficient phagocytosis [86], while FcγRIIIb signals to the nucleus for nuclear factor activation [84] and for NETs formation [78]. Therefore, in principle, a particular cell response could be induced or inhibited by engaging or blocking the corresponding FcγR. Information similar to the one described for neutrophil Fcγ receptors on other immune cells, such as monocytes or

This work was supported by Grant 254434 from Consejo Nacional de Ciencia y

dendritic cells, is not available. Future research is needed in this area.

**34**
