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Home | Pregnancy Timeline | News Alerts |News Archive Sep 11, 2013

 

immune response proposal

Proposed mechanisms in cancer-associated myositis.
(A) Initiation of antitumor response. The immune system targets highly expressed or mutated antigens in tumor cells at early stages during cancer development. This response is either effective (resulting in resolution of the tumor without clinical symptoms) or ineffective (tumor growth). (B) Initiation of muscle inflammation. Normal healthy skeletal muscle does not express autoantigens shared by cancer or regenerating muscle in appreciable levels (light pink cells). (C) Following injury, however, regenerating muscle cells express high levels of antigens targeted in the antitumor response. These cells are targets for CD8+ T cells, which have antitumor function, and which damage muscle (brown cells). (D) Damage of regenerating cells provides additional antigen to DCs, driving autoreactive lymphocytes, and causing additional waves of repair. Recruitment of inflammatory cells and cytokine production induces additional fiber damage and muscle regeneration, producing the antigen drive necessary for propagation of the immune response. Repeated cycles of inflammation, injury, and repair with sustained expression and persistence of antigen results in dual targeting of both tumor and muscle cells by the immune system. Abbreviations: B, B cell; CD4+ T or CD8+ T denotes a CD4-positive or CD8-positive T cell; DC, dendritic cell; IFN, interferon; mDC, myeloid dendritic cell; MHC, major histocompatibility complex; NK, natural killer cell; TCR, T-cell receptor.

Image credit: FIGURE 3 Proposed mechanisms in cancer-associated myositis.




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How immune system kills healthy cells

Medical scientists at the University of Alberta have made a key discovery about how the immune system kills healthy cells while attacking infections. This finding could one day lead to better solutions for cancer and anti-viral treatments.

Faculty of Medicine & Dentistry researcher Colin Anderson recently published his team’s findings in the peer-reviewed journal, Journal of Immunology. His team included colleagues from the United States and the Netherlands, and graduate students from the U of A.

Previous research has shown that when the immune system launches an aggressive attack on infected cells, healthy tissues and cells can be killed or damaged in the process. Anderson and his team discovered the mechanisms in the immune system that cause this “overkill” response.

“This opens the opportunity that one might be able to manipulate the immune system response to block collateral damage without blocking the killing of infected cells,” Anderson explained.

“In the future this might be important in the development of clinical treatments in cases where the immune system response needs to be harnessed. For example, in treating various viral infections, the collateral damage caused during the immune system attack is a large part of the illness.

“In other cases, such as cancer or tumour treatments, one may want to increase the immune system’s ability to kill collateral cells, in hopes of killing tumour cells that would otherwise escape during treatment and spread elsewhere in the body. Our research suggests there are other mechanisms that could improve cancer therapy and make it more efficacious. This finding could also help us understand why certain cancer treatments are more successful than others.”


For years, it was assumed the weaponry to kill infected cells versus healthy cells was exactly the same. Anderson’s team discovered: “the weaponry the immune system uses to try and kill an infected or cancerous cell is not exactly the same as the weaponry that causes collateral damage to innocent bystander cells that aren’t infected.”


The research group is continuing the work in this area to see if they can indeed alter the level of collateral damage to healthy cells without altering the attack on infected cells.

Abstract
An ongoing dilemma faced during an immune response is generating an effective, often proinflammatory response to eliminate pathogens and/or infected cells while also minimizing collateral damage to adjacent noninfected tissues. The factors limiting bystander cell injury during an Ag-specific immune response in vivo are largely unknown. In this study, using an in vivo model of islet transplants in TCR transgenic mice, we show that both CD4 and CD8 T cells do have the capacity to inflict adjacent tissue damage and that this injury is greatly enhanced in sensitized hosts. CD4 T cell–mediated killing of specific and bystander cells occurred via different mechanisms. Unlike specific target cell killing, CD4-mediated bystander injury required tissue Fas expression and was inhibited with anti–IFN-γ Ab treatment in vivo. Moreover, bystander cell injury was not entirely nonspecific but rather required, in naive recipients, that the MHC allele expressed by the bystanders was self. Importantly, the coinhibitor programmed death-1 plays an important role in restraining bystander cell injury mediated either by defined TCR transgenic T cells or by polyclonal T cell populations. Thus, the differential requirements for specific versus bystander cell injury suggest that there are opportunities for inhibiting immune pathology without compromising Ag-specific immunity in vivo.

Anderson is a researcher in the Department of Surgery and the Department of Medical Microbiology and Immunology. He is also a member of both the Alberta Diabetes Institute and the Alberta Transplant Institute.

This work was supported by Canadian Institutes for Health Research Grant FRN79521 and an award from the Alberta Heritage Foundation for Medical Research (to C.C.A.), as well as by studentships from the Muttart Diabetes Research and Training Center/Alberta Diabetes Institute (to G.T.).

Original press release: http://www.med.ualberta.ca/news/2013/september/immune-system-findings