Your browser is too old
We can't provide a great video experience on old browserUpdate now
General Features of Immune Response to Microbes
This Sqadia video provide comprehensive details about Immunity to Microbes Especially Bacteria. General features of immune response to microbes are that they provide defense against microbes is mediated by the effector mechanisms of innate and adaptive immunity. The immune system responds in distinct and specialized ways to different types of microbes to most effectively combat these infectious agents. The survival and pathogenicity of microbes in a host are critically influenced by the ability of the microbes to evade or resist the effector mechanisms of immunity. In many infections, tissue injury and disease may be caused by the host response to the microbe and its products rather than by the microbe itself. In General Scheme of an Immune Response Pathogen with non-self-proteins damages the epithelium to break through the epithelial barrier. Cytokines and Chemokines are a diverse collection of soluble proteins and peptides that modulate the behaviour of cells and Conceptually similar to hormones. However, cytokines and chemokines are not exclusively produced by organised cells located in glandular tissue. They show many biological activities. Chemokines largely associated with chemoattraction of other cells. The activities of cytokines and chemokines often overlap with other cytokines and chemokines.
Innate Immunity to Extracellular Bacteria
Extracellular bacteria are capable of replicating outside host cells. They cause disease by two principal mechanisms: They induce inflammation, which results in tissue destruction at the site of infection. Many of these bacteria produce toxins: Endotoxins and Exotoxins. The immune responses against extracellular bacteria are aimed at eliminating the bacteria and at neutralizing the effects of their toxins. The principal mechanisms of innate immunity to extracellular bacteria are: Complement activation, Phagocytosis and Inflammatory response. Complement activation leads to opsonization and enhanced phagocytosis of bacteria. Complement by-products stimulate inflammatory response by recruiting and activating leukocytes Phagocytes use surface receptors (mannose receptors, scavenger receptors), to recognize extracellular bacteria. Phagocytes use Fc receptors and complement receptors to recognize opsonized bacteria. Generation of C5 convertase leads to the activation of the Lytic Pathway.
Adaptive Immunity to Extracellular Bacteria
Humoral immunity is the principal protective immune response against extracellular bacteria: Functions to block infection, eliminate the microbes, neutralize toxins. Adaptive immune responses to EC microbes consists of:- Antibody production and Activation of CD4+ helper T cells. Humoral immunity is a major protective immune response against extracellular bacteria, and it functions to block infection, to eliminate the microbes, and to neutralize their toxins. Antibody responses against extracellular bacteria are directed against cell wall antigens and secreted and cell-associated toxins, which may be polysaccharides or proteins. The polysaccharides are prototypic thymus-independent antigens, and humoral immunity is the principal mechanism of defense against polysaccharide-rich encapsulated bacteria. The effector mechanisms used by antibodies to combat these infections include neutralization, opsonization and phagocytosis, and activation of complement by the classical pathway. Neutralization is mediated by high-affinity IgG, IgM, and IgA isotypes, the latter mainly in the lumens of mucosal organs; opsonization by some subclasses of IgG; and complement activation by IgM and subclasses of IgG.
Immunity to Intracellular Bacteria
Intracellular bacteria survive and even replicate within phagocytes. These microbes are able to find a niche where they are inaccessible to circulating antibodies. Their elimination requires the mechanisms of cell-mediated immunity. The innate immune response to intracellular bacteria is mainly mediated by:- Phagocytes and Natural Killer (NK) cells. Mice with severe combined immunodeficiency, which lack T and B cells, are able to transiently control infection with the intracellular bacterium Listeria monocytogenes by NK cell-derived IFN-γ production. However, innate immunity usually fails to eradicate these infections, and eradication requires adaptive cell-mediated immunity. Viral infections cause an immunological disequilibrium that provokes CD8 T cell responses. These cells play critical roles in purging acute infections, limiting persistent infections, and conferring life-long protective immunity. At every stage of the response anti-viral CD8 T cells are sensitive to signals from cytokines.
Immunity Against Fungi/Parasites
In Immunity against Fungi the principal mediators of innate immunity against fungi are neutrophils and macrophages. Dendritic cells activated via this lectin receptor produce TH17-inducing cytokines, such as IL-6 and IL-23. The Th17 cells stimulate inflammation, and the recruited neutrophils and monocytes destroy the fungi. Cell-mediated immunity is the major mechanism of adaptive immunity against fungal infections. Balancing protection and immunopathology in fungal infections: a cooperative effort of the innate and adaptive immune systems. Candida albicans is the most commonly encountered fungal pathogen of humans and is frequently found on the mucosal surfaces of the body. Host defense against C. albicans is dependent upon a finely tuned implementation of innate and adaptive immune responses, enabling the host to neutralise the invading fungus. Fungal immune evasion. Fungal immune evasion is the process by which fungi avoid and antagonize the fungal host response, which is mediated by the host's immune system.