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    Home > Active Ingredient News > Immunology News > How does the body's immune system protect itself when a new coronavirus invades? The SARS-CoV-2 immune response is that things.

    How does the body's immune system protect itself when a new coronavirus invades? The SARS-CoV-2 immune response is that things.

    • Last Update: 2020-07-22
    • Source: Internet
    • Author: User
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    The novel coronavirus (SARS-CoV-2), which is now in the Wuhan, has been developing in the world in the end of 2019. It has spread to the whole country and has become a worldwide epidemic disease in Qian Hongfa. (China Medicine University).but so far, there are no effective anti-virus drugs.in front of the virus, people can only sit and wait for death. No, in fact, the best "doctor" is in your body, which is your immune system.let's talk about how the body resists the invasion of new coronavirus, which comes from my protection.first of all, let's analyze the structure of the new coronavirus. Viral structure: nucleocapsid: composed of genomic RNA and phosphorylated nucleocapsid protein (n). Two membrane proteins: membrane (m) protein and membrane (E) protein. Two kinds of spike proteins: spike glycoprotein pruning molecule (s) and hemagglutinin esterase (he) * * here we pay attention to S protein, which is the main weapon of virus invasion.after the two viruses invade the human body, the immune system starts the innate immune response to resist the virus.in this process, macrophages recognize antigens and phagocytize the components of the host's innate immune system, and detect virus infection by using pattern recognition receptors (PRRS) to recognize pathogen related molecular patterns (PAMPs) · Immature dendritic cells (DCS) have a strong ability to phagocytize antigens. They differentiate into mature DCs when they ingest antigens or are stimulated by some factors. Mature DCs express high levels of costimulatory factors and adhesion factors. Activated macrophages can activate NK cells to kill viruses. Let's explore the mechanism of innate immunity Toll like receptor (TLR) is one of the main types of PRRS. It can recognize the S proteins on the surface of virus, such as tram and Tirap, and recruit trif molecule and MyD88 molecule to TLR receptor; MyD88 recruits kinase irak4 to activate downstream NF KB and MAPKs pathways; trif recruits kinase TRAF6 to activate downstream NF KB and IRFs pathways; irak4 interacts with TRAF6, resulting in k-63 ubiquitination To promote the ubiquitination of NEMO to activate NF - kbnf - κ B pathway and IRFs to recruit inflammatory nuclear factors, promote gene expression of interleukin, interferon and tumor necrosis factor, and produce related cytokines.· the virus s glycoprotein binds to ACE2 receptor on the cell surface and enters the cell.TLR and RIG-I-like receptor (RLR) can recognize viral RNA and activate trif molecule · Protein kinase PKC mainly exists in the cytoplasm. When cells are stimulated, PKC shifts from the cytoplasm to the cell membrane in a Ca2 + dependent manner, and then activates the functions of cytokines in MAPK and NF KB pathways: 1. Activating complement; 2. Conditioning; 3. Inhibiting virus replication; 4. Promoting antigen processing; 5. Initiating adaptive immune response.after the initiation of three innate immunity, the specific immune response is triggered by innate immunity (I) · PRR (mannose receptor, scavenger receptor) on the surface of antigen-presenting cells (APC) recognizes PAMP → mediates APC phagocytosis and uptake of pathogens (antigenic presentation) → provides the first activation signal of T cells · TLR on APC surface recognizes PAMP → activates intracellular signal transduction → up regulates the expression of MHC-II molecules and costimulatory molecule B7 → provides the second activation signal of T cells. · TLR → starts intracellular signal transduction → induces the expression of cytokines (such as IL-12, chemokines, etc.) and promotes naive T cells to differentiate into different subtypes. Let's focus on the mechanism of CD4 + T cell differentiation Co receptor: TCR recognizes the antigen presented by MHCII molecules, at the same time, receptor crosslinks → CD4 molecules bind to MHCII molecules, causing CD4 molecules to be close to TCR in space → tyrosine phosphokinase Lck connected with intracellular segment of CD4 molecules phosphorylates tyrosine on CD3 molecular chain → causes ZAP70 and Fyn to collect near membrane receptor and be activated by Lck → then activate PLC through DAG and IP3 pathways The transcription factors NF KB and NF at are activated respectively, then they are transferred into the nucleus and act on the transcription and synthesis of related gene sequences Costimulatory molecules: the binding of B7 and CD28 can activate PI-3K → the signal, together with ZAP70, Fyn, activates Ras MAPK pathway → FOS / IU gene expression. The two molecules form a dimer, namely transcription factor AP-1 → AP-1 interacts with NF-AT → IL-2 gene transcription. Therefore, in the absence of costimulatory signal, the synthesis of IL-2 is blocked → T cells are incompetent.differentiation mechanism of four cell immune CD8 + T cells. At the same time of Th cell differentiation, APC infected by virus can directly activate CD8 + T cells without Th cell assistance.→ → innate immunity initiates specific immune response (2) · Th cell dependent (indirect activation) APC surface expresses antigen peptide / mhci molecular complex and antigen peptide / MHCII molecular complex at the same time, presenting antigen to CD4 and cd8t cells; → CD4 + T cells and CD8 + T cells need to recognize the specific antigen presented by the same APC+ T cells provide IL-2 or stimulate APC to express costimulatory molecules, which assist CD8 + T cells to activate, proliferate and differentiate into cytotoxic T cells.we will analyze the mechanism of cellular immunity. Specific recognition and binding stage: effector target cells specifically bind to TCR peptide of CTL through adhesion molecules / mhci (target cell) · polarization of CTL: TCR and co receptor targeting target site aggregation → cytoskeleton, subcellular structure and cytoplasmic granules rearrange and distribute to target cells Lethal attack stage: 1. Perforin / granzyme pathway: perforin → target cell necrosis; granzyme → target cell peri death; 2. FasL / Fas and TNF / TNFRI pathways: target cell apoptosis; 5. Humoral immune B cell differentiation mechanism Activation signal 1 (antigen recognition signal) BCR specifically binds to B cell epitope of antigen; CO receptor: CD21 / CD19 / CD81 recognizes C3d on antigen molecule; lgal / LG β: signal transduction · Activation signal 2 (costimulatory signal) activation of initial th: APC (DC) provides double signals and CK to the initial CD4 T cells to activate, proliferate and differentiate into effector Th cells; → → innate immunity initiates specific immune response (3) B cell presents antigen: B cell absorbs antigen through BCR, processes into peptide, and interacts with MHC IL-1 (APC) and IL-4 (Th2) promote the activation of B cells.after B cells produce antibodies, the antibodies enter the body fluid and produce the following effects. Humoral immune mechanism 1. Antibody 1. Conditioning effect: refers to the role of antibodies and complement in promoting phagocytes to phagocytize virus and other antigens.FC of IgG binds to FCR of phagocytes.ADCC can specifically bind IgG to the corresponding antigen determinant on the surface of target cells → NK cells bind to FC segment of LGG bound to target cells with the help of its fcyr Ⅲ → activated NK cells release cytotoxic substances such as perforin and granzyme to kill target cells → target cell apoptosis II. Complement 1. Cytolysis effect mac makes target cell membrane perforation and cell apoptosis 2. Conditioning action C3b adsorption disease About 3.8 billion years ago, the earliest life appeared on the earth. In the following several billion years, the living things on the earth were interdependent, and the human immune system was gradually improved due to the existence of external pathogens.in the face of pneumonia caused by the new coronavirus, do a good job of self-protection. in addition, it is also important to pay attention to healthy diet and exercise. In the absence of specific drugs and vaccines, the best doctor is your immune system. when you see your immune system desperate in the face of an invasive virus, why not take care of your body. see the message area for download of PDF version of complete sars-cov-2 immune response pathway map.
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