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How The Immune Response Quickly Becomes
Tailored To Suit the Assault ?
Nature of the invading pathogen offense
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This means that different chemical structures and microenvironmental cues need to be detected and
initiating the most effective response strategy
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Although these recognition molecules are Membrane-bound receptors, soluble receptors or
secreted recognition molecules can also be engaged
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The outcome of this Ligand binding is an
intracellular or extracellular cascade of events that ultimately leads to the labeling and destruction of
the pathogen—simply referred to as the immune response
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The nature of the immune response will vary depending on the number and type of recognition
molecules engaged
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The majority of their life cycle residing inside host cells
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This means
that some immune cells must be capable of detecting changes that occur in a host cell after it becomes
infected
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In this case, recognition molecules positioned inside cells are key to the initial response
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This sacrifice is for the good of the whole organism, in
some instances it can cause disruptions to normal function
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These cells are called helpers because they guide the behavior of other
immune cells, including B cells, and are therefore pivotal for selecting the pathway taken by the immune
response
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Therefore , The resulting immunodeficiency allows opportunistic infections to take hold
and potentially kill the patient
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These rely primarily on cell surface or soluble recognition
molecules that probe the extracellular spaces of the body
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For instance, antibodies can squeeze into spaces in the body
where B cells themselves may not be able to reach, helping to identify pathogens hiding in these out-ofreach places
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In such cases these cells can deposit toxic substances or that can secrete products that induce
expulsion (e
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, sneezing, coughing, vomiting) become a better strategy
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At the same time, these various immune carry out their jobs with considerable overlap in structure and
in function
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The offender and tailor the subsequent immune response
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How Pathogen Recognition Molecules Can Be Encoded
As Genes or Generated by DNA Rearrangement ?
Most pathogens express at least a few chemical structures that are not found in mammals
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It is these unique antigenic structures that the immune system
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For example, encapsulated bacteria possess a polysaccharide coat with a unique chemical structure that
is not found on other bacterial or human cells
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When PRRs detect these chemical structures, a
cascade of events labels the target pathogen for destruction
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These conserved proteins are found in
one form or another in many different types of organism, from plants to fruit flies to humans, and
represent a first line of defense for the quick detection of many of the typical chemical identifiers
carried by the most common invaders
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A significant and powerful corollary to this is that it allows early categorizing or profiling of the sort of
pathogen of concern
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For example, viruses frequently expose unique chemical structures only during their replication inside
host cells
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This can trigger an immediate antiviral response in the infected
cell that blocks further virus replication
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Host-pathogen interactions are an ongoing arms race; pathogens evolve to express unique structures
that avoid host detection, and the host recognition system co-evolves to match these new challenges
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The host immune response would quickly become obsolete thanks to
these real-time pathogen avoidance strategies
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To favor randomness in the design of some recognition molecules strategy, called generation of
diversity, is employed only by developing B and T lymphocytes
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This feat is accomplished by
rearranging and editing the genomic DNA that encodes the antigen receptors expressed by each B or T
lymphocyte
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Thus, B and T cells make surface receptors unique to each individual, which are then not passed on to
offspring
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(Generation of diversity and clonal selection in T and B lymphocytes
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Different clones Of B cells (numbered 1, 2, 3,
and 4)
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These clonal selection occurs when one of these cells encounters its cognate or specific antigen
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The B cells secrete antibody, a
soluble form of the receptor, reactive with the activating antigen
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the latter activated T
cells, which secrete cytokines that aid in the further development of adaptive immunity, and cytotoxic T
lymphocytes (CTLs), which can kill infected host cells
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This theory, proposed by Polly Matzinger at
the National Institutes of Health
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Therefore, cell death can
have many causes, including natural homeostatic processes, mechanical damage, or Infection
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This should not and normally does not activate an
immune response
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The host damage or danger-associated compounds released in these situations, collectively
referred to as alarmins, can engage specific host recognition molecules (e
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, the same PRRs that
recognize PAMPs) that deliver a signal to immune cells to get involved during these unnatural causes of
cellular death
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Therefore this theory, including the coincidence between exposure to some infectious agents and the
development of autoimmunity (immune reactivity against host structures)
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The danger or damage model of self-tolerance postulates that the immune response is not
activated when host cell death occurs safely, but only when this death is accompanied by
damage- or danger-associated signals produced

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