Abstract
The integrin associated protein (CD47) is a widely and moderately expressed glycoprotein in all healthy cells. Cancer cells are known to induce increased CD47 expression. Similar to cancer cells, all immune cells can upregulate their CD47 surface expression during infection. The CD47-SIRPa interaction induces an inhibitory effect on macrophages and dendritic cells (dendritic cells) while CD47-thrombospondin-signaling inhibits T cells. Therefore, the disruption of the CD47 interaction can mediate several biologic functions. Upon the blockade and knockout of CD47 reveals an immunosuppressive effect of CD47 during LCMV, influenza virus, HIV-1, mycobacterium tuberculosis, plasmodium and other bacterial pneumonia infections. In our recent study we shows that the blockade of CD47 using the anti-CD47 antibody increases the activation and effector function of macrophages, dendritic cells and T cells during viral infection. By enhancing both innate and adaptive immunity, CD47 blocking antibody promotes antiviral effect. Due to its broad mode of action, the immune-stimulatory effect derived from this antibody could be applicable in nonresolving and (re)emerging infections. The anti-CD47 antibody is currently under clinical trial for the treatment of cancer and could also have amenable therapeutic potential against infectious diseases. This review highlights the immunotherapeutic targeted role of CD47 in the infectious disease realm.
Highlights
The CD47 is expressed on both hematopoietic and non-hematopoietic cells and plays crucial role in immune regulation and maintenance of homeostasis [1,2,3]
Poxvirus has been shown to encode expression of CD47-like protein and this strongly inhibits the activation of macrophages and T cells
Addition to its effective antitumor function, the antibody does not cause anemia in an in vivo setting [77]. All these CD47-blocking antibodies unanimously show a similar immunological effect resulting in increased phagocytosis and activation of antigen presenting cells, increased proliferation and activation of cytotoxic CD8 T cells during tumor and viral infections
Summary
The CD47 is expressed on both hematopoietic and non-hematopoietic cells and plays crucial role in immune regulation and maintenance of homeostasis [1,2,3]. Varieties of cancer cells are known to induce increased CD47 surface expression as a mechanism to evade macrophage mediated phagocytosis [9,10,11]. The CD47-SIRPa interaction induces an antiphagocytic signal in macrophages and dendritic cells This interaction leads to the recruitment and activation of Src homology phosphate (SHP-1 and SHP-2) thereby inhibiting the myosin-IIA and this results in prevention of phagocytosis [12,15]. The disruption of CD47/SIRPa-signaling increases macrophage mediated phagocytosis of diseased vascular tissue and cancer cells This leading to regression of much different type of tumors both in vivo and in vitro [24,25,26,27,28,29]. We recapitulate anti-CD47 antibody as a potential therapeutic target for infectious diseases
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