Intro To Immune I & Ii (Foundations Exam 1)

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immunity

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resistance or protection against infectious agents (e.g. bacteria, fungi, viruses)

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immunogen

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something (antigen) that is capable of evoking an immune response such as the production of antibodies

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immunology

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the study of the cellular and molecular events that occur during the host response to a foreign substance

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immune response

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the combined repertoire of cellular and molecular events that occur during exposure to foreign substances

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major function of immune system

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protect individuals against infection by pathogenic microorganisms

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innate immunity

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- "born with it"
- exists prior to exposure to a foreign substance or pathogen
- not improved by repeated exposure
- not antigen specific
- no "memory"

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adaptive immunity

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- developed as a result of exposure to foreign substance or pathogen
- specific for particular antigen
- enhanced by repeated exposure
- immunological "memory"

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physical components of innate immunity

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skin, mucus, coughing, sneezing, crying, urination, competition for space and nutrients by host normal flora

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biochemical components of innate immunity

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- complement: lysis, opsonization, chemotaxis
- lysozyme
- low pH (acidity)
- interferons

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cells of innate immunity

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phagocytes (neutrophils, monocytes, macrophages, dendritic cells), NK cells,, many others

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physical components of adaptive immunity

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none

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biochemical components of adaptive immunity

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- antibody
- cytokines ( IL-2, IFN-gamma, IL-4, IL-5, IL-10)

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cells of adaptive immunity

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B & T lymphocytes
dendritic cells

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innate immunity mechanism

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1. epithelial surfaces (skin, lungs, GI tract, reproductive tract)
--> physical barriers with anti-microbial properties
2. complement system
--> plasma proteins with anti-microbial properties --> activated in response to infection
3. tissue-resident and circulating immune cells
--> macrophages, neutrophils, DC, with capacity to kill microbes and initiate inflammatory response

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complement system

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circulating molecules function in an enzymatic cascade to:
1. induce inflammation --> local increase in fluid (plasma and WBCs)
2. opsonize pathogens --> promote uptake by macrophages and neutrophils
3. induce lysis --> direct killing of microbes or infected cells
-activated by multiple mechanisms

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macrophages

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- tissue-resident in CT, mucosal tissues, liver, etc
- derived from monocytes
- long-lived and present at onset of infection
- initiate response and serve many roles

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neutrophils

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- polymorphonuclear (PMN) leukocytes
- short-lived (~2 days)
- abundant cells of circulation
- "flood" into sites of infection (inflammation) and engulf and kill microbes

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inflammation

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- major effector mechanism of innate
- initiated by complement, cytokines, and other means
- increases vascular permeability
- increases lymph flow
- helps recruit effector cells
- generally beneficial

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important cytokines produced by macrophages in response to bacterial products

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IL-6, TNF-alpha, IL-1beta, CXCL8, IL-12

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IL-6

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systemic effects: fever, induces acute-phase protein production by hepatocytes

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TNF-alpha local effects

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local effects: increases vascular permeability (activates vascular endothelium), increased entry of complement and cells, increase fluid drainage to lymph nodes

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TNF- alpha systemic effects

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fever, mobilization of metabolites, shock

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IL-1beta local effects

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- activates vascular endothelium
- activates lymphocytes
- local tissue destruction increases access of effector cells

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IL-1beta systemic effects

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fever, production of IL-6

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CXCL8 local effects

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chemotactic factor recruits neutrophils and basophils to site of infection

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IL-12 local effects

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activates NK cells

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Toll-like receptors

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(pattern recognition receptors)
- recognize pathogen-associated molecular patterns
- increase microbe-killing capacity of phagocytes
- increase cytokine secretion
- induction of virus resistant state (Type I interferon)
- enhance ability to activate adaptive immunity

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NOD-like receptors (NLR)

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(pattern recognition receptors)
- interaction with microbial ligands produces multiple downstream signals -- typically pro-inflammatory

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phagocyte activation

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TLRs and NLRs cause activation of cells:
- induce inflammatory response
- increase killing capacity of phagocytes, cytokines, virus resistance, and better activation of adaptive immunity

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type I interferons (IFN)

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- anti-viral system in most cells types
- detect virus infection
- interferons secreted and act in autocrine and paracrine fashion
- activate anti-viral state
--> shut off protein synthesis, activate RNAse, become better Natural Killer cell targets

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features of adaptive immunity

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1. specificity
2. adaptability
3. self/non-self discrimination
4. memory

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B lymphocytes

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- make antibodies which act as antigen receptors
- differentiate into antibody secreting cells called plasma cells

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T lymphocytes

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- express T cell receptors (TCRs) that bind antigen

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T helper (Th) cells (CD4+)

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- secrete numerous cytokines
- activate DCs
- help B lymphocytes in producing antibodies

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T cytotoxic (Tc) (CD8+) cells

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- destroy virus-infected cells and tumor cells

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T regulatory (Treg) cells

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- regulate immune responses by controlling the activities of other immune cells including T cells

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antigen presenting cells (APCs)

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- ingest, process, and present antigen in the form of peptides that are recognizable by T cells
--> **DCs, macrophages, and B cells

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clonal selection

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- lymphocytes have distinct specificity for antigen prior to contact with antigen --> random rearrangement of antigen receptor genes
** cells capable of responding to self antigens (auto-reactive) are destroyed following contact with self antigen (during development) or rendered unresponsive (in adults)

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phases of antibody production

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1. lag phase: time between initial exposure and detection of antibodies (4-7 days)
2. exponential phase: rapid increase in amount of circulating antibodies due to increase in number and activity of plasma cells
3. steady state (plateau) phase: rate of antibody synthesis is equivalent to rate of degradation
4. declining phase: antibody synthesis wanes as immunogen (pathogen) is eliminated

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characteristics distinguishing primary from secondary immune response

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1. shorter lag time in secondary response, extended plateau, and slower decline in antibody levels
2. antibody titer is higher in secondary response
3. IgG is major antibody in secondary response--IgM is major antibody in primary response
4. binding affinity of antibodies is higher in secondary response--> "affinity maturation"

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mechanisms of antibody response

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1. neutralization of bacteria and their toxic products
2. opsonization of pathogens to facilitate uptake and destruction by phagocytes
3. complement activation to cause bacterial destruction

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antibody structure

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- two copies each of heavy chain and light chain
- divalent
- variable (V) region binds antigen (combination of heavy and light chains)
- constant region (Fc) mediates effector functions

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generation of antibody diversity

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- multiple DNA gene segments encode variable region
- segments randomly recombine
- one segment of each type is used to create a functional gene
- pairing of variable heavy and light chains
- imprecise joining of segments
- recombining segments encode variable region of antibody

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IgM

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- exists in serum as pentamer (10 total binding sites)
- mostly confined to bloodstream
- expressed on naive B cells
- does NOT cross placenta
- predominant antibody during first week of infection
- strong activator of complement

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IgG

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- principal Ig of serum
- 4 subclasses in humans
- longest half-life
- only antibody able to cross placenta
- provides fetal immunity up to 1 year after birth
- opsonic activity
- activator of complement
- neutralization of toxins and viruses

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IgA

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- most abundant Ig in body when mucosal surfaces are included
- exists as monomer (serum) and dimer (secretory IgA)
- predominant form of Ig in sero-mucus secretions
- secretory IgA protects mucosal regions
- IgA in breast milk is transferred to gut of newborn
- neutralizing anitbody

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IgE

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- extremely low concentration in serum
- important in allergic reactions (binds to Fc receptor of mast cells and basophils)
- induced in response to parasitic infections such as worms