Abstract: Monoclonal antibodies against human Mac-1 are provided. These antibodies can bind to different states of Mac-1 so as to alter the biofunctions of Mac-1. These antibodies can modulate Th1/Th2 cytokine secretions by TLR-activated immune cells and can be used for the treatments of diseases related to acute and chronic inflammatory disorders, such as infectious diseases, and cancers.

Abstract: Provided are an anti-CD11b antibody or an antigen-binding portion thereof, and methods and use of the antibody for modulating immunoresponses by regulating CD11b expression on cells.

Abstract: A pharmaceutical composition for boosting an immune response contains TREM-like transcript-1 (TREML1) extracellular domain (ECD) or stalk polypeptide. The TREML1 ECD or stalk polypeptide is derived from human or mouse TREML1. The pharmaceutical composition further contains an antigen as a vaccine, wherein the TREML1 ECD or stalk polypeptide functions as an adjuvant or immune booster.

Abstract: A method for reversing immune suppression or immune exhaustion or for treating a disease associated with immune suppression includes: administering a composition to a subject in need of such treatments, wherein the composition contains a CD11b modulator that binds specifically to CD11b on a cell to inhibit PD-L1 expression. The CD11b modulator is an antibody or an antigen-binding portion thereof, or a compound as described.

Abstract: A hepatitis B virus (HBV) vaccine includes an HBV core antigen (HBcAg) and/or HBV surface antigen (HBsAg) formulated in nanocomplexes. The nanocomplexes contain chitosan and ?-PGA. These nanocomplexes containing HBc/sAg, chitosan, and ?-PGA can induce more balanced T helper cells (Th1 and Th2) polarization than can a conventional vaccine with an alum adjuvant. HBc/s-NC of the invention can elicit high levels of antibodies against HBsAg, a rapid elimination of HBsAg, and a slow decrease of HBeAg, indicating a phenomenon of HBsAg seroconversion. Thus, HBc/s-NC can overcome immune tolerance caused by chronic HBV infection to re-establish host immunity leading a functional cure.

Abstract: A pharmaceutical composition for use in treating hepatitis B virus (HBV) infection includes an effective amount of an antibody against CD11b or a binding fragment thereof. A method for treating hepatitis B virus infection includes administering to a subject in need thereof an antibody against CD11b. Anti-CD11b antibody binding to CD11b may trigger immunostimulatory responses, as evidenced by the following observations: increased surface expression of MHC II and CD86 in CD11b+ peripheral blood mononuclear cells (PBMCs); suppressed level of hepatitis B surface antigen (HBsAg) and HBV DNA in the blood; and accelerated clearance of HBV from liver.

Abstract: The present invention relates to methods for modulating immune response based on binding I-domain of CD11b on the tumor associated myeloid cells (TAMCs) in the tumor microenvironment. Particularly, binding to I-domain of CD11b with anti-CD11b-I-domain antibody triggers immunostimulatory environment that have one or more of the following effects in the tumor microenvironment: increase the inflammatory cytokine in the tumor microenvironment, decrease the population of IDO+ myeloid suppresser cells, up-regulate M1 marker over M2 marker on the tumor associated macrophage, increase M1:M2 tumor associated macrophage ratio, promote differentiation of dendritic cells (DC), nature killer dendritic cells (NKDC), and plasmacytoid dendritic cells (pDC), increase population of 4?1BB+PD?1+ neoantigen specific CD8 T cells. Converting cold (non-inflamed) to hot (inflamed) tumor by binding to I-domain of CD11b with anti-CD11b-I-domain antibody allows enhanced effectiveness of immune response modulator.