Myeloid cells are recruited to damaged tissues where they can resolve infections and tumor growth or stimulate wound healing and tumor progression. Recruitment of these cells is regulated by integrins, a family of adhesion receptors that includes integrin CD11b. Previous studies on tumor inflammation revealed that immune cell adhesion receptors play unique but critical roles during tumor progression. CD11b/CD18 has been shown to mediate macrophage adhesion, migration, chemotaxis and accumulation during inflammation. Accordingly, a need exists for novel methods of treating cancer that utilize the role that integrin CD11b plays during inflammation.
Researchers at UC San Diego have demonstrated that modulation of integrin CD11b activity can be used as a cancer immunotherapy approach by harnessing the macrophage polarization towards tumor-suppressing phenotype (and away from tumor promoting phenotype associated with tumor associated macrophages (TAMs). Basically, this is a method of treating cancer by administering CD11b modulator/agonist, CD11b modulator is an antibody, small molecule etc. and CD11b modulator alters the polarization of macrophages.
This is a method of treating cancer by administering CD11b modulator/agonist, CD11b modulator is an antibody, small molecule etc. and CD11b modulator alters the polarization of macrophages.
The invention is based on studies that CD11b signaling inhibits immune suppression, modulates neovascularization and promotes anti-tumor immune responses in models of murine and human cancer.
This technology is patent pending and UC San Diego is seeking companies interested in commercializing this technology.
Cancer growth, immune response, immune suppression, inflammation, CD11b, CD18, tumor progression