The Immune Response to Infectious Agents
•Télécharger en tant que PPT, PDF•
12 j'aime•3,913 vues
![The Immune System ,[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
Recommandé
Contenu connexe
Tendances
Tendances (20)
Similaire à The Immune Response to Infectious Agents
Similaire à The Immune Response to Infectious Agents (20)
Plus de Bruno Mmassy
Plus de Bruno Mmassy (20)
Dernier
Dernier (20)
The Immune Response to Infectious Agents
- 1. The Immune Response to Infectious Disease By: Prof M.I.N. Matee Head, Department of Microbiology and Immunology, MUCHS
- 6. Agents That Cause Disease. Pathogens Viruses Bacteria Parasites Fungi
- 12. CD8 + T and CD4 + T
- 13. CTL activating macrophage function
- 40. Quote of the day “ Why leave the tail……. … .if you ate the rest of the cow.”
Notes de l'éditeur
- Host defenses against viral infection aim to first slow viral replication and then eradicate infection.
- INFs function to inhibit viral replication. . IFNα and IFNβ produced by virally infected cells defuse to adjoining cells and activate genes that interfere with viral replication. INF-alpha and INF-beta also stimulate production of MHC class I molecules NK cells may be one of the principal mechanisms of immunity against viruses early in the course of infection, be fore more specific immune responses have developed. NK cells also effectively recognize and lyse infected cells in which the virus may have inhibited antigen presentation and class I MHC expression IFN α and IFN β can enhance the ability of NK cells to lyse infected target cells, limiting viral infection
- Most viruses express surface receptor molecules that enable them to initiate infection by binding to host cell molecules. If antibody is produced to the viral receptor, it can block infection altogether by preventing binding of viral particles to host cell. IgA in mucus secretions plays an important role in host defense against viruses by blocking viral attachment to mucosal epithelial cells Neutralizing antibodies bind to envelope or capsid proteins and prevent viral attachment and entry into host cells. IgG appears to be the most active isotype against viruses. Opsonizing antibodies may enhance phagocytic clearance of viral particles. Secondary immunoglobulins of the IgA isotype may be important for neutralizing viruses that enter via respiratory or intestinal tract. If the induced antibody is of a compliment-activating isotype, lysis of envelope virion can happen. Antibody or compliment can also agglutinate viral particles and functions an oposonizing agent to facilitate Fc or C3b receptor-mediated phagocytosis of the viral particles.
- CD8 + T c cells require cytokines produced by CD4 + T h 1 cells. Activated T h 1 cells produce a number of cytokines, including IL-2 , INF-γ, and TNF. These cytokines either directly or indirectly, defend against viruses. INF-γ acts directly by inducing an antiviral state in cells. IL-2 acts indirectly by assisting in the activation of CD8 + T c cell precursors into an effector population. Both IL-2 and INF-γ activate NK cells, which play an important role in host defense during the first days of many viral infections. CD4 + T cells also produce important cytokines to stimulate inflammatory responses at sites of viral infection and activate macrophage function.
- CD8 + T c cells recognize endogenous synthesized cytosolic viral antigens in association with class I MHC molecules on any nucleated cell (antigen presenting cell APC), thus represents an important component of the specific immune response against infections.
- A persistent infection with some viruses can cause the formation of circulating immune complexes composed of viral antigens and specific antibodies. These complexes deposit in the blood vessels and lead to systemic vasculitis. Some viruses are known to contain amino acid sequences that are also present in host self cells, leading to an immune response to self
- Despite their restricted genome size, a number of viruses have been found to encode proteins that interfere at various levels with specific or innate host defenses. By blocking or inhibiting the antiviral proteins induced in uninfected cells, viruses have been shown to over come the antiviral effect of interferons. By secreting a protein that binds the c4b complement component, inhibiting the classical complement pathway or by binding to the c3b complement component, inhibiting both the classical and alternative pathway.
- Continual antigenic variation, by either antigenic drift or antigenic shift, results in the frequent emergence of new infectious strains of the virus. by: direct viral infection of the lymphocytes or macrophages, suppressing cytokine production, and by suppressing class I MHC.
- , e.g., in the circulation, in extracellular connective tissues, and in various tissue spaces such as the airways genitourinary tract, and intestinal lumens. ., resulting in tissue destruction at the site of infection which are components of bacterial cell walls ., which are actively secreted by the bacteria.
- , an immunogenic component of the cell walls and capsules of these pathogens. Polysaccharides are prototypical thymus-independent antigens that directly stimulate B cells (Abbas, 1991).
- caused by cytokines produced mainly by activated macrophages. . Septic shock is the most severe cytokine-induced pathologic effect of infection by gram-negative and some gram-positive bacteria.
- Despite their restricted genome size, a number of viruses have been found to encode proteins that interfere at various levels with specific or innate host defenses. By blocking or inhibiting the antiviral proteins induced in uninfected cells, viruses have been shown to over come the antiviral effect of interferons. By secreting a protein that binds the c4b complement component, inhibiting the classical complement pathway or by binding to the c3b complement component, inhibiting both the classical and alternative pathway.
- , e.g., in the circulation, in extracellular connective tissues, and in various tissue spaces such as the airways genitourinary tract, and intestinal lumens. ., resulting in tissue destruction at the site of infection which are components of bacterial cell walls ., which are actively secreted by the bacteria.
- Innate immunity is ineffective in controlling colonization by and spread of these microorganisms NK cells produce IFN-γ, which in turn activates macrophages and promotes killing of phagocytosed bacteria. NK cell provide an early defense against intracellular bacteria, prior to the development of specific immunity
- Protein antigens of intracellular bacteria stimulate CD4+ and CD8+ T cells. CD4+ T cells respond to intracellular antigens presented by class II MHC expressed on APCs. Intracellular bacteria are potent inducers of the differentiation of CD4+ helper T cells to the TH1 phenotype. The cytokines produced in the innate immune response to intracellular bacteria, IL-2 by macrophages and IFN-γ by NK cells; also promote the development of TH1 cells that secretes IFN-γ. IFN-γ activates macrophages to produce reactive oxygen species and enzymes that kill phagocytosed bacteria. If the bacteria survive within cells and release their antigen into the cytoplasm, they stimulate CD8+ CTLs activation and they function by producing more IFN-γ and by killing any macrophages that may be harboring bacteria in the cytoplasm (Abbas, 1991).
- The localized concentration of lysosomal enzymes in the granulomas can cause extensive tissue necrosis
- Macrophages are also capable of combating fungal infections.
- Fungi often cause specific antibody responses, which are useful for serological diagnosis. However, the protective efficacy of humoral immunity is not established
- Humans are usually infected by bites from infected intermediate hosts or by sharing a particular habitat with an intermediate host.
- This may be due to the loss of surface molecules that bind complement or acquisition of host regulatory proteins such as decay accelerating factor (DAF).
- CD4+ T cell –derived cytokines activate macrophages. A special type of antibody-dependent cellular cytotoxicity (ADCC), in which IgE antibodies bind to the surface of the helminth, eosinphils then attach to Fc receptors. The eosinophils are activated to secrete granule enzymes that destroy the parasites. These responses are attributed to the propensity of helminthes to stimulate the TH2 subset of CD4+ helper T cells, which secrete IL-4 and IL-5. IL-4 stimulates the production of IgE, and IL-5 stimulates the development of eosinophils.
- The granulomas serve to contain the parasite, but severe fibrosis associated with this chronic cell-mediated immune response leads to disruption of venous blood flow in the liver, portal hypertension, and cirrhosis
- Helminthic parasites can reside in intestinal lumens and are sheltered from cell-mediated immune responses As the parasite travels through the host, it encloses itself in a glycolipid and glycoprotein coat derived from the host, masking the presence of its own antigens This resistance is due to a biochemical change in the surface coat.
- Helminthic parasites can reside in intestinal lumens and are sheltered from cell-mediated immune responses As the parasite travels through the host, it encloses itself in a glycolipid and glycoprotein coat derived from the host, masking the presence of its own antigens This resistance is due to a biochemical change in the surface coat. In stage specific variation the mature tissue stages of parasites produce different antigens from the infectious stage. In continuous variation of major surface antigens each replication of the parasite produces a new variation of the parasites surface antigens.
- If pathogens are able to breach the innate immune system, the specific immune system is capable of defending the host against infection by means of humoral and/or cell-mediated immune response. If you take into account the number of pathogens present, there are few pathogens that the immune system is incapable of handling, unless the pathogen has ability to suppress the immune system. Although scientist have learned much about the immune system, they continue to study how the body launches attacks that destroy invading microbes, infected cells, and tumors while ignoring the healthy tissue. New technologies for identifying individual immune cells allow scientists to determine which targets are triggering an immune response. The combination of new technology and expanded genetic information will teach us more about how the body protects itself from disease.