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Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and also Disease. 5th edition. New York: Garland also Science; 2001.
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Many type of of the bacteria that reason transmittable illness in human beings multiply in theextracellular spaces of the body, and the majority of intracellular pathogens spcheck out by relocating fromcell to cell through the extracellular fluids. The extracellular spaces are defended bythe humoral immune response, in which antibodies developed by B cells causethe destruction of extracellular microorganisms and proccasion the spread of intracellularinfections. The activation of B cells and also their differentiation right into antibody-secretingplasma cells (Fig. 9.1) is prompted by antigenand also normally needs helper T cells. The term ‘helper T cell’ is frequently offered to suppose acell from the TH2 class of CD4 T cells (view Chapter 8), but a subset of TH1 cells can additionally help inB-cell activation. In this chapter we will certainly therefore use the term helper Tcell to suppose any equipped effector CD4 T cell that deserve to activate a B cell. HelperT cells likewise regulate isoform switching and have a function in initiating somatichypermutation of antibody variable V-region genes, molecular processes that wereexplained in Chapter 4.
The humoral immune response is mediated by antibody molecules that aresecreted by plasma cells. Antigen that binds to the B-cell antigen receptor signals B cells and is, atthe very same time, internalized and processed into peptides that activate armedhelper (more...)
Antibodies add to immunity in 3 primary ways (see Fig. 9.1). To enter cells, virsupplies and also intracellular bacteriabind to certain molecules on the target cell surface. Antibodies that bind to thepathogen deserve to proccasion this and are shelp to neutralize the pathogen. Neutralization by antibodies is also crucial inavoiding bacterial toxins from entering cells. Antibodies protect against bacteriathat multiply external cells greatly by facilitating uptake of the pathogen by phagocyticcells that are specialized to destroy ingested bacteria. Antibodies carry out this in either oftwo methods. In the initially, bound antibodies coating the pathogen are recognized by Fc receptors on phagocytic cells that bind to the antibody consistent C region (see Section 4-18). Coating the surchallenge of a virus toenhance phagocytosis is called opsonization. Conversely, antibodies binding to the surchallenge of a microorganism canactivate the proteins of the complement mechanism, which was defined in Chapter 2. Complement activationoutcomes in match proteins being bound to the pathogen surchallenge, and these opsonizethe pathogen by binding match receptors on phagocytes. Other enhance componentsrecruit phagocytic cells to the site of infection, and also the terminal components ofmatch can lyse certain microorganisms straight by developing pores in their membranes.Which effector mechanisms are involved in a details response is identified by theisokind or course of the antibodies developed.
In the first component of this chapter we will certainly define the interactions of B cells withhelper T cells that bring about the production of antibodies, the affinity maturation ofthis antibody response, the isoform switching that confers functional diversity, and thegeneration of memory B cells that provide long-lasting immunity to reinfection. In therest of the chapter we will certainly discuss in detail the mechanisms through which antibodies containand eliminate infections.
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ContentsB-cell activation by equipped helper T cellsThe distribution and also functions of immunoglobulin isotypesThe damage of antibody-coated pathogens via Fc receptorsOverview to Chapter 9General referencesSection references
By agreement through the publisher, this book is available by the search function, yet cannot be browsed.