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 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.

Abstract: A method fits reversing immune suppression or immune exhaustion or for treating a disease associated with immune suppression includes: administering a co position 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: The present invention discloses a method for inhibiting the growth of Mycobacterium tuberculosis, comprising: administering at least one selective binding agent such as an anti-CD13 antibody or a CD13 antagonist which can bind a CD13 receptor of a cell to inhibit infection of Mycobacterium tuberculosis. Administration of anti-CD13 antibody can reduce an expression level of the CD13 receptor, inhibit entry of Mycobacterium tuberculosis into monocytes, reduce survival of Mycobacterium tuberculosis in monocytes, and kill Mycobacterium tuberculosis effectively.

Abstract: Disclosed is a method for treating a symptom of M. tuberculosis infection in a subject, comprising administering the patient with an effective amount of (3R,4S)-1-(4-fluorophenyl)-3-[(3S)-3-(4-fluorophenyl)-3-hydroxypropyl]-4-(4-hydroxyphenyl)zetidin-2-one (EZETIMIBE). In the preferred embodiments, EZETIMIBE is capable of significantly inhibiting the survival and proliferation of Mycobacterium tuberculosis in the monocytes. The anti-tuberculous effect of EZETIMIBE is partly through stimulating CD13 leading to monocytes activation and thus bacterial killing of Mycobacterium tuberculosis, and partly through depleting the intracellular nutrition necessary for the survival of Mycobacterium tuberculosis. It is also proved that EZETIMIBE is capable of directly killing Mycobacterium tuberculosis outside cells.

Abstract: Disclosed is a method for treating a symptom of M. tuberculosis infection in a subject, comprising administering the patient with an effective amount of (3R,4S)-1-(4-fluorophenyl)-3-[(3S)-3-(4-fluorophenyl)-3-hydroxypropyl]-4-(4-hydroxyphenyl)zetidin-2-one (EZETIMIBE). In the preferred embodiments, EZETIMIBE is capable of significantly inhibiting the survival and proliferation of Mycobacterium tuberculosis in the monocytes. The anti-tuberculous effect of EZETIMIBE is partly through stimulating CD13 leading to monocytes activation and thus bacterial killing of Mycobacterium tuberculosis, and partly through depleting the intracellular nutrition necessary for the survival of Mycobacterium tuberculosis. It is also proved that EZETIMIBE is capable of directly killing Mycobacterium tuberculosis outside cells.

Abstract: The present invention discloses a method for inhibiting the growth of Mycobacterium tuberculosis, comprising: administering at least one selective binding agent such as an anti-CD13 antibody or a CD13 antagonist which can bind a CD13 receptor of a cell to inhibit infection of Mycobacterium tuberculosis. Administration of anti-CD13 antibody can reduce an expression level of the CD13 receptor, inhibit entry of Mycobacterium tuberculosis into monocytes, reduce survival of Mycobacterium tuberculosis in monocytes, and kill Mycobacterium tuberculosis effectively.