| Autor: |
Yi-Hsin Lee, Kuo-Wang Tsai, Kuo-Cheng Lu, Li-Jane Shih, Wan-Chung Hu |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
Biomedicines, Vol 10, Iss 10, p 2497 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
2227-9059 |
| DOI: |
10.3390/biomedicines10102497 |
| Popis: |
Host immunological pathways are delicate to cope with different types of pathogens. In this article, we divide immunological pathways into two groups: Immunoglobulin G-related eradicable immunities and Immunoglobulin A-related tolerable immunities. Once immune cells encounter an antigen, they can become anergic or trigger immune reactions. Immunoglobulin D B cells and γδ T cells are recognizing self-antigens to become anergic. Immunoglobulin M B cells and αβ T cells can trigger host immune reactions. Eradicable immune responses can be divided into four groups: TH1/TH2/TH22/THαβ (TH—T Helper cell groups). Tolerable immune responses can be divided into four groups: TH1-like/TH9/TH17/TH3. Four groups mean hosts can cope with four types of pathogens. Cancer is related to immune dysfunction. TH1-like immunity is pro-tumor immunity and THαβ is anti-tumor immunity. TH1-like immunity is the host tolerable immunity against intracellular micro-organisms. THαβ immunity is the host eradicable immunity against viruses. Cancer is also related to clonal anergy by Immunoglobulin D B cells and γδ T cells. Oncolytic viruses are related to the activation of anti-viral THαβ immunity. M2 macrophages are related to the tolerable TH1-like immunity, and they are related to metastasis. This review is key to understanding the immune pathogenesis of cancer. We can then develop better therapeutic agents to treat cancer. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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