MindMap Gallery Medicine-Pathogen Infection Mechanism_backup_282260
This is a mind map about the mechanism of pathogenic infection_backup_282260. It is introduced in detail and described comprehensively. I hope it will be helpful to those who are interested!
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
Staphylococcus aureus
antigen
Immunogenicity: refers to the ability of an antigen to stimulate the immune system to produce a specific immune response. Immunoreactivity: refers to the ability of an antigen to specifically bind to a response product.
Route of transporting antigens: 1. Most tissue-derived antigens enter lymph nodes through afferent lymphatic vessels, and then flow into the subcapsular sinus of lymph nodes. Small molecule soluble antigens can reach the B cell area through the duct between the subcapsular sinus and the underlying follicle. 2. Subcapsular sinus
immune system
Lymphocyte recirculation and lymphocyte homing: Lymphocyte recirculation causes lymphocytes settled in the periphery to enter the thoracic duct from the efferent lymphatic vessels and enter the blood circulation. After reaching the lymph nodes, they pass through high endothelial cell venules and are redistributed in peripheral immune organs or The repetitive cyclical process of an organization. Lymphocyte recycling gives lymphocytes more opportunities to contact antigens and APCs to initiate adaptive immune responses.
Innate immunity (non-specific immunity)
process
Anatomical barrier: The skin is a huge physical barrier. Most pathogens cannot invade intact skin. The pH value of the skin is also slightly acidic, which can delay the growth of pathogenic microorganisms.
Mucosal immunity: Mucosal epithelial cells are an integral part of the innate immune system, participating in the response to pathogens and capable of delivering antigens to immune cells. Epithelial cells can prevent antigenic substances with larger diameters from entering. Mucosal immunity affects various environmental and immune signals, thereby altering the function of the mucosal barrier.
Acute inflammatory response: Pathogens usually enter the human body through mucous membranes or epithelial tissues. Acute inflammatory response is usually the first response to the invasion of such antigens and is the blocking response of the innate immune system to the invasion of external antigens. Vascular endothelial cells in the damaged epithelial barrier are activated, release cytokines and other inflammatory mediators, induce endothelial cells to express adhesion molecules such as selectins, and mediate the extravasation of phagocytes. Neutrophils are the first cells to bind to endothelial cells that undergo an inflammatory response and extravasate into the tissue, reaching a peak within 6 hours of infection. Subsequently, the extravasated neutrophils release mediators, and monocytes, macrophages, and eosinophils are chemoattracted and infiltrate into the inflammatory site after 5 to 6 hours. After endothelial cells are damaged, an acute inflammatory response occurs.
Characteristics: Accumulation of white blood cells, plasma proteins, and fluid extracted from the blood at extravascular tissue sites of infection or injury. Leukocytes and plasma proteins normally circulate in the blood and are recruited to sites of infection and injury to perform a variety of effector functions, killing microorganisms and repairing tissue damage. The most abundant leukocytes recruited from the blood to sites of acute inflammation are neutrophils, and important plasma proteins that enter sites of inflammation include complement proteins, antibodies, and acute phase reactants. The accumulation of these blood-borne components into sites of inflammation relies on reversible changes in blood vessels in infected or damaged tissue, all of which are induced by mediators such as cytokines.
Cytokines: Highly active and multifunctional small molecule substances secreted by activated cells. They mainly mediate and regulate immune responses and inflammation.
Temperature: When an inflammatory response occurs in a Staphylococcus aureus-infected wound, cytokines may systematically alter the hypothalamic temperature set point, leading to inflammation in the body.
Adhesion molecules: (The recruitment of white blood cells and plasma proteins from the blood to sites of infection and tissue damage is a major process in the inflammatory response). The homing and recruitment of leukocytes requires the temporary adhesion of leukocytes to the vascular endothelium. This process is mediated by a series of molecules on the surface of leukocytes and vascular endothelial cells that promote intercellular adhesion. This series of molecules is called adhesion molecules.
Identifying characteristics: PAMP and DAMP. PAMPs can recognize pathogen-associated molecular patterns, including structural components of microorganisms or corresponding products. These components and products are usually necessary for the survival of microorganisms but are not expressed in mammals. 1. Microbial-specific nucleic acids. 2. Characteristic proteins present in microorganisms, such as N-formylmethionine in bacterial proteins. 3. Lipopolysaccharide in Gram-negative bacteria, lipoteichoic acid, mannose residues in Gram-positive bacteria, etc. DAMP is a damage-related molecular pattern released by dead or damaged cells. It is a structural component unique to damaged or dead cells and does not exist in normal body cells. Apoptotic cells are not released. Can enhance the body's innate immune response to infection. The innate immune system recognizes the unique molecular patterns of S. aureus and the dead or damaged cells it infects.
Adaptive immunity (specific immunity)
Cytokines
Antibodies (B lymphocytes)
Antibody: an important effector molecule that mediates humoral immune response. It is a globulin secreted by B lymphocytes after they proliferate and differentiate into plasma cells under the stimulation of effective antigens, and can specifically bind to the corresponding antigen.
Immunoglobulin Ig: A globulin with antibody activity or a chemical structure similar to that of an antibody. Antibodies are immunoglobulins, but that doesn't hold true anyway.
Structure: The basic structure is two identical heavy chains (H chains) with larger relative molecular masses and two identical light chains (L chains) with smaller relative molecular masses. The heavy chains and light chains are separated by The interchain disulfide bonds form a symmetrical "Y"-shaped structure. Heavy chains can be divided into five categories based on differences in immunogenicity of the constant regions, and they are respectively involved in the composition of five types of immunoglobulins. Light chains can be divided into two categories based on their immunogenicity. The part with the most drastic sequence changes in the variable region is called the hypervariable region. The hypervariable regions of VH and VL together form the antigen-binding site, which determines the specificity of the antibody and is responsible for recognizing and binding antigens. This region forms a spatial conformation complementary to the antigenic epitope, also known as the complementarity determining region. The hypervariable region is also the idiotype or idiotype antigenic determinant of the Ig. The amino acid sequence of the region outside the hypervariable region is relatively conservative and is called the "backbone region", which can stabilize the configuration of the complementarity-determining region and facilitate the binding of the complementarity-determining region to the antigenic epitope. Constant region refers to the same type of antibodies produced by individuals of the same species against different antigens. Although the V regions are different, the amino acid sequence of the C region is relatively constant and has the same immunogenicity. Hinge region: facilitates binding of two epitopes by two arms J chain: Connect Ig monomers at the carboxyl end of the H chain to form dimers or multimers. Secretory patch SP: synthesized and secreted by mucosal epithelial cells, and binds to CH2 of dimeric IgA through covalent bonds, making it secretory IgA. After sIgA is secreted onto the mucosal surface, it exerts mucosal immunity. SP can cover the hinge region and protect it from hydrolysis by proteolytic enzymes. Papaya hydrolase: It can hydrolyze the antibody at the amino terminus of the interchain disulfide bond in the hinge region of the heavy chain, forming two identical monovalent antigen-binding fragments and one crystallizable fragment. Pepsin:
Antigen characteristics: Immunogenicity refers to the ability of an antigen to stimulate the immune system to produce a specific immune response. Immunoreactivity refers to the ability of an antigen to specifically bind to immune response products.
Diversity: isotypes, allotypes, and unique types.
Biological activity: 1. Specific binding to antigens. Antibodies have the function of neutralizing toxins and blocking the invasion of pathogens, that is, neutralization. However, they cannot dissolve or kill target cells carrying antigens and require complement or phagocytes. effect to clear antigens or pathological damage. 2. Activate complement. 3. Opsonization: refers to the fact that the antibody that binds to the granular antigen binds to the FcR on the surface of phagocytes through the Fc segment, activating macrophages and enhancing their phagocytic killing ability, and the "bridging" of the antibody enables the granular antigen to be anchored to the phagocyte. On the surface, it is easier to be swallowed. 4. Antibody-dependent cell-mediated cytotoxicity ADCC: refers to that after the IgG binds to the target cell antigen, its Fc segment can bind to the FcgR of effector cells such as NK cells, macrophages, and monocytes to promote the release of cytotoxic particles. , causing target cell lysis. 5. Mediate type I hypersensitivity reactions.
Characteristics and functions of five types of antibodies
B lymphocytes
Development and maturity of B cells: During this period, progenitor B cells begin to rearrange their Ig heavy chain genes, but the light chain genes have not yet begun to rearrange, and begin to express Igα and Igβ. Pre-B cells begin to express an alternative light chain, which combines with the μ chain to form the pre-B cell receptor, which is a surface marker of pre-B cells and can promote B cell proliferation. Pre-B cells continue to develop, complete Ig light chain gene rearrangement, and form mIgM expression and cell surface. The B cell antigen receptor complex composed of mIgM and Igα/Igβ heterodimer is a surface marker of immature B cells. Immature B cells undergo negative selection and continue to develop into mature B cells. The simultaneous expression of mIgM and mIgD molecules is a surface marker of mature B cells, and the variable regions of these two mIg are exactly the same.
Negative selection (clearance): Negative selection occurs at the immature B cell stage. If the mIgM expressed by it can bind to the multivalent self-antigen on the surface of bone marrow stromal cells, it can cause mIgM cross-linking, leading to apoptosis of immature B cells, that is, It is clonal clearance; if it binds to a monovalent soluble self-antigen, it will cause the expression of mIgM to be down-regulated. Although these cells can enter peripheral immune organs, they do not respond to antigen stimulation, which is called clonal incompetence. In addition, some immature B cells that recognize self-antigens can change the specificity of their B cell antigen receptors through receptor editing.
Ig gene rearrangement
process Heavy chain gene rearrangement: A heavy chain D gene segment is combined with a J gene segment, and the spacer sequence between the two is removed to form a DJ segment. Next, a V gene fragment is combined with a rearranged DJ fragment to form a functional V gene that encodes the variable region of the heavy chain of an Ig molecule. Further translation. After heavy chain gene rearrangement is completed, light chain gene rearrangement begins. Light chain gene rearrangement: Usually the IGK gene starts to rearrange first. If it fails, the IGL gene rearranges next, but this order is not absolute. The V gene fragment is directly recombined with the J gene fragment to form the V gene encoding the variable region of the light chain of the Ig molecule. Subsequently, the V gene is recombined with the C gene fragment of the light chain gene to form an mRNA encoding the light chain, which is further translated into the light chain of an Ig molecule.
Exclusion: Allelic exclusion and isotype exclusion are used to ensure the single specificity of B cell clones and the expression of only one Ig type light chain.
Ig class switching: Class switching of mature B cells is the second gene rearrangement of the Ig gene, also known as isotype switching. It means that the variable region of an Ig molecule remains unchanged, but the type of its heavy chain changes. B cells that undergo class switching can differentiate into plasma cells and memory B cells that produce IgG, IgA, or IgE antibodies.
The mechanism of Ig diversity generation: 1. Combination diversity. 2. Connect diversity. 3. Receptor editing. 4. High-frequency mutations in somatic cells.
B lymphocyte activation The specific antigen signal is the first signal for B cell activation, and the co-receptor complex can enhance the first signal. The first signal can upregulate the expression of MHC class II molecules and costimulatory molecule B7 in B cells, enhancing the ability of B cells to activate Th cells. Costimulatory signal is the second signal of B cell activation. Activated Th cells can inducibly express CD40L, and CD40L interacts with CD40 on the surface of B cells to provide the strongest second signal for B cell activation. If the second signal is missing, the B cells will not only fail to be activated by the first signal, but will enter a state of incompetence. Cytokines promote B cell activation. T cell nucleus B cell interaction: Specific B cells and T cells must come into contact with each other to generate a strong antibody response. Specific T cells and B cells must meet and interact at the edge of the T cell area through specific chemotaxis in order to initiate normal humoral immunity.
Proliferation and differentiation of B cells (mainly in germinal centers) Extrafollicular activation of B cells: Extrafollicular activation of B cells initiates an early response to protein antigens and establishes a germinal center response. B cells are activated after recognizing antigens in lymph follicles, and some of them enter the extrafollicular area of peripheral lymphoid tissue, differentiate into IgM-producing plasma cells, secrete IgM antibodies, and participate in the body's immediate defense response. Affinity antibodies produced by extrafollicular activated B cells can limit the spread of infection. Extrafollicular responses also contribute to the generation of follicular helper T cells. Four to seven days after the initiation of T cell-dependent B cell responses, a small number of B cells activated outside the follicles migrate back to the follicles and proliferate rapidly, forming "germinal centers." The germinal center is formed by the clonal expansion of one or several antigen-specific B cells and is divided into light and dark areas. The formation of these structures depends on the presence of FDC and the interaction between Tfh's CD40L and B-cell CD40.
Class switching: During the TD-Ag response, after activation of B cells expressing IgM and IgD, some progeny cells change the constant region of the heavy chain and produce antibodies containing different classes of heavy chains, but the specificity of the antibody remains unchanged. This process is class switching or isotype switching. Bacteria and viruses activate T cells to produce cytokines, promoting the conversion of IgM into IgG, while parasite infections activate T cells to produce IL-4, producing humoral immunity dominated by IgE antibodies. Staphylococcus aureus activates T cells to produce cytokines, which promotes the conversion of IgM into IgG types, resulting in class switching.
complement
Basic concept: It is widely involved in the body's defense response to microorganisms and immune regulation. It is one of the main effector mechanisms of humoral immunity and an important effector mechanism of innate immunity. Complement is mainly synthesized and secreted by hepatocytes, macrophages, intestinal epithelial cells and other tissue cells. It is unstable in nature and is especially sensitive to heat. Heating at 56°C for 30 minutes can inactivate complement. Usually inactive proteins that become activated under specific conditions.
activation pathway
Classical pathway: The earliest discovered complement activation pathway, which mainly functions in the middle and late stages of primary infection. Mainly activated by antigen-antibody complexes, IgM or IgG binds to the corresponding antigen, and there must be two or more Fc regions binding to C1. It is divided into startup phase, activation phase and effect phase.
Alternative pathway: It is the oldest form of complement activation, plays a role in early infection or primary infection, and is an important effector mechanism of innate immunity.
Mannan-binding lectin pathway
Biological activity: 1. Lyse bacteria and cells. 2. Conditioning effect. 3. Mediate inflammatory response. 4. Clear immune complexes. 5. Immunomodulatory effect.
MHC (T lymphocyte)
MHC
Genetic characteristics: 1. Haplotype inheritance and co-dominance. 2. Polymorphism. 3. Linkage disequilibrium: refers to the phenomenon that the probability of alleles belonging to two or more gene loci appearing on the same chromosome is different from the expected value.
Classification
Classic HLA class I and HLA class II genes: The expression products have the function of antigen presentation, directly participate in the activation and differentiation of T cells, and participate in the regulation of adaptive immune responses. Class I is located in a segment far away from the centromere and includes three functional groups, mainly involved in endogenous antigen presentation and immune regulation. Class II is located in a segment close to the centromere and is mainly involved in exogenous antigen presentation and immune regulation respectively.
Non-classical HLA class I genes Antigen processing-related genes: 1. PSMB gene, involved in the processing of endogenous antigens. 2. Antigen processing-related transporters, involved in the transport of antigen peptides in endogenous antigen processing. 3. HLA-DM plays a positive regulatory role in the processing and presentation of exogenous antigens. 4. The HLA-DO gene plays a negative regulatory role in the processing and presentation of exogenous antigens. HLA class III genes
Molecular Structure
HLA class I molecules are composed of α chain and β chain linked by non-covalent bonds. The beta chain is encoded by a gene on human chromosome 15. The β chain has no transmembrane region and intracellular region, but only an extracellular region. Alpha chains are transmembrane molecules. The structures of α1 and α2 constitute the antigen-binding groove, which can bind antigen peptides and also become a "polymorphic region". Their structural differences determine the differences in immune response functions of different individuals; α3 and β chains constitute the immunoglobulin-like region, which maintains The configuration of the entire HLA class I molecule, among which α3 can bind to the CD8 molecule on the surface of T cells and promote the activation of CD8 molecules; the extended part of α3 forms the transmembrane region and the cytoplasmic region. The basic function is to present endogenous antigen peptides through the antigen-binding groove for recognition by CD8 T cells, thereby initiating an immune response mediated by CD8 T cells. Both ends are closed, and the length of the accepted antigen peptide is limited. It is widely distributed on the surface of nucleated cells in the body. Not expressed in red blood cells (nucleated).
HLA class II molecules are heterodimeric glycoproteins composed of α chain and β chain. Both α chain and β chain are transmembrane proteins, and each extracellular region has two domains. Among them, α1 and β1 constitute the antigen-binding groove, which combines and accommodates the antigen peptides produced by APC processing, also known as the polymorphic region; α2 and β2 constitute the immunoglobulin-like region, maintaining the molecular configuration, and β2 can also bind to the T cell surface. CD4 molecules promote the activation of CD4 T cells. Extended portions of the α2 and β2 domains form the transmembrane region of class II molecules. The basic function is to bind exogenous antigen peptides through the antigen-binding groove and present them to CD4 T cells for recognition, thereby initiating CD T cell-mediated immune responses. The distribution in the body is limited and mainly distributed on the surface of specific cells, such as professional APCs (DCs, macrophages and B cells), thymic epithelial cells and activated T cells.
Binding to antigenic peptides has certain selectivity. The specific site on the antigen peptide that can interact with the antigen-binding groove of the HLA molecule is called an anchor site. The amino acid residues located at anchor positions are called "anchor residues". The anchoring position and anchoring residues determine how strongly the HLA antigen-binding groove binds to the antigenic peptide.
Biological functions: 1. Present antigens, participate in adaptive immune responses, determine the MHC restriction of T cells recognizing antigens, participate in the selection and differentiation of T cells in the thymus, determine individual differences in disease susceptibility, and participate in the formation of population immunity. Heterogeneity of response, involved in transplant rejection. 2. As regulatory molecules, they participate in the innate immune response. The classic MHC class III genes encode complement components and participate in the inflammatory response to kill pathogens. The gene products of non-classical MHC class I molecules and MIC serve as activating receptors or inhibitory receptors for NK cells. Ligand regulates the killing function of NK cells.
T lymphocytes
T cell antigen receptor complex: A TCR complex consists of a TCR molecule and a CD3 molecule.
TCR: It is a heterodimer and a member of the immunoglobulin superfamily. αβTCR: It consists of α chain and β chain, which can be divided into three parts: extracellular region, transmembrane region and intracellular region. The two peptide chains are covalently bonded through the disulfide bond in the extracellular region. The extracellular regions of the α chain and β chain each contain a variable region at the far membrane end and a constant region at the proximal membrane end. The variable region of each chain contains three regions with the most concentrated amino acid sequence variation, called complementarity determining regions, namely CDR1, CDR2 and CDR3. Among them, CDR3 has the largest variation, which directly determines the antigen of the T cell antigen receptor. Specificity. The transmembrane regions of the α chain and β chain are composed of hydrophobic amino acids and contain positively charged amino acid residues, which can non-covalently bind to the negatively charged amino acid residues in the transmembrane region of the CD3 molecule to form a TCR-CD3 complex. . γδTCR: Similar in structure, but not as diverse as αβTCR.
Stages of T cell maturation 1. Double negative cell stage: DN cells are T cells before pre-T cells. At this time, T cells express neither CD4 nor CD8 molecules. It does not express T cell antigen receptors and CD3 molecules, cannot recognize antigens, and does not have any functions. Progenitor T cells begin to rearrange T cell antigen receptor genes, which is the branch point of αβ and γδ T cell differentiation. The TCRβ chain completes gene rearrangement, but the α chain genes have not yet been rearranged. The β chain expressed by αβ T cells and the α chain of pre-T cells form pre-T cell antigen receptors. Cells expressing pre-T cell antigen receptors are pre-T cells. Under the induction of cytokines such as IL-7, pre-T cells actively proliferate, express CD4 and CD8 molecules, and continue to enter the DP cell stage. 2. DP cells complete α gene rearrangement and assemble with β chains to form T cell antigen receptors. At this time, cells expressing T cell antigen receptors are immature T cells. Immature T cells undergo positive selection and further differentiate into SP cells. 3. Single-positive cell stage: SP cells undergo negative selection and further develop into MHC-restricted, self-tolerant mature T cells, which enter peripheral immune organs through blood circulation.
αβ gene rearrangement: Once the T cell antigen receptor gene is successfully rearranged and expressed, genetic changes will no longer occur, and its function and affinity will no longer change.
Positive selection: occurs in the deep layers of the thymic cortex and involves interactions between immature T cells and intracortical epithelial cells. Only DP cells that bind with the appropriate affinity to the self-antigen peptide-MHC class I/II molecule complex on the surface of thymic epithelial cells can survive, continue to develop into SP cells, and acquire the ability to recognize the restriction of their own MHC in the process of antigen recognition. . Negative selection: occurs at the junction of cortex and medulla and in the medulla area. The positively selected SP cells interact with the self-antigen peptide-MHC class I molecules or MHC class II molecule complexes on the surface of DCs, macrophages and other cells there. The SP cells that bind with high affinity undergo apoptosis and are eliminated. It ensures that the T cell pool entering peripheral immune organs does not contain T cells directed against self-antigens, eliminates self-reactive T cells, and obtains self-tolerance.
immune response process
Antigen processing and presentation and T cell recognition of antigen (sensing stage)
T cells have dual recognition of antigens, not only recognizing antigen peptides, but also recognizing MHC molecules.
Exogenous antigen processing and presentation pathway (MHC class II molecules form complexes and present them to CD4 T lymphocytes for recognition) Uptake and processing of exogenous antigens: Exogenous antigens are taken up by APC, and the endocytosed antigens are surrounded by the cell membrane to form vesicles. During the process of migrating into the cells, the pH value gradually decreases. Bodies, eventually called late endosomes, fuse with lysosomes to form phagolysosomes. Under the action of lysosomal tissue hydrolase, the antigen in the endosome is degraded into antigenic peptides containing 13 to 18 amino acids. Synthesis and transport of MHC class II molecules: The α and β chains of MHC class II molecules are synthesized in the rough endoplasmic reticulum and folded into dimers. Peptide-bearing of MHC class II molecules: In the MIIC region, HLA-DM binds to MHC class II molecules, causing conformational changes in the MHC class II molecules. CLIP is removed from the groove of the MHC class II molecules until a high-affinity short peptide binds to it. In the groove, HLA-DM dissociates from MHC class II molecules. In this process, HLA-DO can competitively inhibit the function of HLA-DM and play a negative regulatory role. Presentation of MHC class II molecules and antigenic peptide complexes.
Endogenous antigen processing and presentation pathway Processing of endogenous antigens. Transport of endogenous antigens. Synthesis, assembly and peptide loading of MHC class I molecules. Presentation of MHC class I molecules and antigenic peptide complexes.
Antigen cross-presentation pathway: Under special circumstances, exogenous antigens are presented to CD8 T lymphocytes for recognition via the MHC class I molecule pathway, while endogenous antigens are presented to CD4 T lymphocytes for recognition via the MHC class II molecule pathway.
Activation, proliferation and differentiation of T cells
Activation, proliferation and differentiation of CD4 T cells
Two signals are required for CD4 T cell activation: The first signal is a necessary condition for T cell activation. After TCR recognizes the antigen peptide-MHC class II molecule complex on the surface of APC, it is transmitted into the cell by the CD3 complex. The CD4 molecule binds to the β2 functional region of MHC class II molecules, which greatly reduces the threshold for TCR to recognize peptide-MHC and plays a role in strengthening the first signal. Therefore, CD4 plays an important role as a co-receptor for T cell activation. The second signal, also called costimulatory signal or costimulatory signal, is provided by the interaction between CD4 T cells and the adhesion molecule pair on the surface of APC. When there is only the first signal but no second signal, the T cells will not only fail to activate, but will enter an incompetent state. When stimulated by the same antigen again, even if the second signal is present, it cannot be activated again. The intercellular adhesion molecules on the cell membrane at the contact point between T cells and APC are arranged in an orderly concentric circle to form a cylindrical structure, which is the immune synapse.
Intracellular signaling of CD4 T cell activation
Proliferation and differentiation of CD4 T cells Under the influence of the first signal and the second signal, CD4 T cells produce IL-2 and other cytokines required for their proliferation and differentiation in an autocrine and paracrine manner, and express their corresponding high-affinity IL-2 receptors. wait. IL-2 stimulates the survival and proliferation of CD4 T cells. The result of proliferation is an increase in the size of antigen-specific clones, that is, clonal expansion. The proliferated CD4 T cells further differentiate into effector helper T cell subsets with different functions under the influence of different cytokines. Under the influence of cytokines IL-12 and IFN-γ, differentiate into Th1 cells, mainly synthesize and secrete IL-2, IFN-γ and TNF-β, activate macrophages, promote their phagocytosis and kill macrophages. Pathogenic microorganisms in the body. Under the action of IL-4, the transcription factors STAT3 and GATA are activated and differentiate into Th2 cells, which mainly synthesize and secrete IL-2, IL-5, IL-6, IL-10 and IL-13, activate B cells, and stimulate IgE Antibodies are produced and mast cells are activated.
Effector function: Recruit and activate phagocytes and other lymphocytes to kill intracellular bacteria and certain extracellular bacteria, and assist B lymphocytes to produce antibodies. It can also activate cells other than phagocytes to kill certain types of pathogens.
CD8 molecule activation, proliferation and differentiation
Activation of CD8 T cells also requires dual signals.
After MHC presents Staphylococcus aureus, it presents it to T cells, causing activation and proliferation of T cells, and in turn stimulates B lymphocytes to produce immune responses.
After the skin is damaged, Staphylococcus aureus enters the body through the damaged surface and destroys endothelial cells. After the mucosal barrier is destroyed, antigens are delivered to immune cells and affect various environmental and immune signals.
After the innate immune system cannot kill all Staphylococcus aureus, Staphylococcus aureus, as an antigen, will induce the proliferation and differentiation of B lymphocytes and enter the humoral immune response stage. After B lymphocytes proliferate and differentiate into mature B cells under the stimulation of effective antigens, they leave the bone marrow and migrate to the B cell area of peripheral immune organs to participate in lymphocyte recycling or receive stimulation from foreign antigens to activate and proliferate and differentiate into plasma cells or Memory B cells. Corresponding antibodies are secreted and specifically bind to Staphylococcus aureus. At the same time, it activates complement, exerts opsonizing and cytotoxic effects, promotes the activation of macrophages, and enhances phagocytic function.
If the skin surface is damaged, resulting in inflammation, or Staphylococcus aureus infected wound